Cards-CAD

Question 1

What is stable angina?

Answer 1

hest pain, pressure, or discomfort that develops with exertion and is relieved with rest. Symptoms often occur when the burden of atheromatous plaque results in fixed coronary stenosis and limitation of blood flow, leading to an imbalance between myocardial oxygen supply and demand.

Question 2

Who should get a coronary CTA?

Answer 2

The use of invasive coronary angiography in patients with stable angina pectoris is generally limited to those with persistent or progressive life-limiting symptoms while on optimal medical therapy or those with high-risk criteria on noninvasive stress testing or coronary CTA

Question 3

How should patients with ischemic CAD first be managed?

Answer 3

Medical therapy should be initiated in all patients with ischemic heart disease. The combination of risk factor modification and medical therapy is referred to as guideline-directed medical therapy

Question 4

What are the two types of medications for CAD?

Answer 4

Medical therapy is divided into two categories: cardioprotective medications and antianginal medications. Cardioprotective medications improve survival, reduce the occurrence of cardiovascular events, and reduce the progression of systemic atherosclerosis. Antianginal medications vasodilate the coronary vasculature or decrease myocardial oxygen demand, thus reducing the frequency and severity of angina pectoris and improving quality of life.

Question 5

What are the cardioprotective medications against CAD?

Answer 5

Aspirin, statin, BB, ACEI, Flu vaccine

These all reduce the risk of CV death

Question 6

What are the abtianginal meds against CAD?

Answer 6

Medications to reduce the frequency and severity of angina pectoris comprise β-blockers, nitrates, calcium channel blockers, and ranolazine.

Question 7

How do beta blockers work as antianginals?

Answer 7

In addition to their cardioprotective effects, β-blockers improve angina pectoris by reducing heart rate, myocardial contractility, and blood pressure, resulting in reduced myocardial oxygen demand.

Question 8

How do nitrates work as antianginals

Answer 8

Nitrates improve myocardial oxygen supply and reduce myocardial oxygen demand by their effects on coronary and systemic vasodilation, respectively. Nitrates have not been proved to reduce the frequency of cardiovascular events (myocardial infarction, death).

Question 9

What are first and second line antianginals?

Answer 9

First: BB and nitrates
Second: CCB

Question 10

How do calcium channel blockers work? What about the nondihydropyridine CCBs?

Answer 10

All calcium channel blockers cause systemic and coronary vasodilation, and nondihydropyridine calcium channel blockers (diltiazem, verapamil) reduce the heart rate.

Question 11

What is first line for Prinzmetal Angina?

Answer 11

Because of their vasodilatory properties, calcium channel blockers are first-line agents for the management of patients with Prinzmetal (variant) angina pectoris.

Question 12

When is ranolazine used for angina?

Answer 12

Ranolazine is a selective inhibitor of the late inward sodium channel in the myocardium. It is generally reserved for patients who remain symptomatic with the use of β-blockers, nitrates, and calcium channel blockers. Ranolazine is an effective antianginal medication; however, its use is limited by cost and adverse effects such as dizziness, headache, nausea, and constipation. Ranolazine should be used with caution in patients with advanced kidney or liver disease and in those taking medications that are potent inhibitors of the CYP3A4 pathway. Examples of strong inhibitors of the CYP3A4 pathway include ketoconazole, clarithromycin, tacrolimus, and cyclosporine.

Question 13

Management MUST HAVES for the treatment of stable angina

Answer 13

**Aspirin or clopidogrel (if aspirin-allergic) is recommended in all patients with established coronary artery disease unless contraindicated; the use of newer antiplatelet agents (prasugrel, ticagrelor) as monotherapy has not been tested in patients with stable angina pectoris.

**All patients with stable angina pectoris should receive a statin and a β-blocker.

**ACE inhibitors are indicated in the treatment of stable angina pectoris, particularly in patients with concomitant diabetes mellitus and left ventricular systolic dysfunction.

Question 14

When should invasive angiography be used?

Answer 14

In patients with stable angina pectoris whose symptoms are not improved with optimal medical therapy, invasive angiography is warranted to define coronary artery anatomy and prepare for revascularization via PCI or coronary artery bypass graft surgery (CABG)

Question 15

What are the two forms of revascularization?

Answer 15

PCI and CABG

Question 16

Who do the guidelines recommend should get PCI?

Answer 16

Current guidelines recommend that diagnostic angiography and PCI be reserved for patients with refractory symptoms while on optimal medical therapy, those who are unable to tolerate optimal medical therapy owing to side effects, or those with high-risk features on noninvasive exercise and imaging tests.

Question 17

Who should get a CABG?

Answer 17

The use of CABG in patients with stable angina is generally indicated only for those who remain symptomatic with optimal medical therapy and have specific angiographic findings (either left main disease or multivessel disease with involvement of the proximal left anterior descending artery), concomitant reduced systolic function, or diabetes mellitus.

Question 18

How should patients who undergo PCI or CABG be monitored? What post-procedure treatments should they have?

Answer 18

Clinical practice guidelines do not recommend the routine use of ECG monitoring, stress testing, or anatomic testing (coronary CTA or invasive angiography) in asymptomatic patients after PCI or CABG.

• ASA should be taken after PCI and CABG indefinitely
• Dual therapy: 1 month after bare metal stent and 6 months after drug eluting stent; 1 year after CABG
• Consider continuing cardioprotective and antianginal meds

Question 19

What is ACS?

Answer 19

It is STEMI, NSTEMI, and unstable angina

Question 20

What is the difference between an NSTEMI and unstable angina?

Answer 20

NSTE-ACSs are characterized by the presence of ischemic chest pain (or an equivalent), the notable absence of ST-segment elevation on ECG, and the presence of either ST-segment depression or T-wave inversion on ECG. In NSTEMI, cardiac biomarkers (serum creatine kinase MB and troponin) are abnormal, whereas in UA, cardiac biomarkers are normal.

Question 21

How is the diagnosis and treatment between STEMI vs. NSTEMI/UA different?

Answer 21

Because the affected artery is completely occluded in STEMI, its diagnosis and treatment are markedly different from those of UA or NSTEMI. For this reason, an initial ECG is imperative in all patients presenting with symptoms consistent with ischemic chest pain, and once diagnosis of STEMI occurs, emphasis is placed on immediate reperfusion of the vessel via thrombolytic therapy or PCI. Patients with ischemic chest pain but without ST-segment elevation on initial ECG are typically classified as having NSTE-ACS and then undergo laboratory testing for cardiac biomarkers. Because these patients do not have an ECG consistent with complete occlusion of a coronary artery and because this group of patients is heterogeneous, risk stratification should occur prior to consideration of coronary angiography and subsequent coronary revascularization with PCI or CABG.

Question 22

When is PCI preferred for a STEMI?

Answer 22

The preferred method of reperfusion for patients with STEMI is primary PCI, especially for patients presenting to hospitals with onsite PCI facilities. Primary PCI is considered appropriate care in patients who present 12 hours or less after symptom onset and in patients who present 12 to 24 hours after symptom onset with severe heart failure, persistent ischemic symptoms, or hemodynamic or electrical instability

Question 23

What happens if someone is still unstable or has symptoms after PCI of culprit artery after a STEMI?

Answer 23

Revascularize the other arteries!

In patients with continued cardiogenic shock after successful PCI of the culprit artery, immediate revascularization of one or more nonculprit arteries is appropriate management.

According to the 2016 multi-society AUC for coronary revascularization, in patients with STEMI in whom the culprit artery has been successfully treated with primary PCI or thrombolysis, it may be appropriate to treat one or more nonculprit artery lesions with PCI or CABG. In these circumstances, patients who may benefit from additional revascularization include those with cardiogenic shock persisting after treatment of the culprit artery; those with spontaneous or easily provoked symptoms of myocardial ischemia; asymptomatic patients with findings of ischemia on noninvasive testing; and asymptomatic patients with intermediate stenosis (50%-70%) and a fractional flow reserve value of 0.80 or less. Fractional flow reserve is the ratio of blood flow distal to the stenosis to blood flow proximal to the stenosis at maximal flow. It is measured during cardiac catheterization by placing a pressure wire across the stenosis and inducing conditions of maximal hyperemia, usually with adenosine.

Question 24

In outside facilities with no PCI… what happens?

Answer 24

Because many patients with STEMI present to hospitals without onsite PCI facilities, a treatment algorithm is typically in place to emergently transfer patients to a PCI-capable facility or administer full-dose thrombolytic therapy. Even when thrombolytic therapy is administered, treatment guidelines recommend that patients be transferred to a PCI-capable facility because of the potential for thrombolytic failure. Failure is like 30-50%

Question 25

What medical therapy is given after a STEMI?

Answer 25

325-mg loading dose of aspirin, supplemental oxygen, therapy to improve symptoms (nitrates, analgesics), therapy to reduce infarct size (β-blockers, ACE inhibitors), and antithrombotic therapy (antiplatelet agents, anticoagulants). Aspirin should be administered immediately; however, the administration of other agents should not delay the plan to reperfuse the infarct-related artery.

Question 26

In a patient with a STEMI, who should you be careful about receiving nitrates or analgesics?

Answer 26

Caution should be used in patients with inferior STEMI and evidence of right ventricular infarction because nitrates and analgesics can lead to reduced preload and significant hypotension.

Question 27

What are the most common post-MI complications during the early management period after STEMI?

Answer 27

The most common complications during the early management period after STEMI are arrhythmias, heart failure, and vascular access issues in patients who undergo primary PCI.

Question 28

How do you manage heart failure and cardiogenic shock after someone has had an MI?

Answer 28

Patients who develop cardiogenic shock after STEMI often have more extensive left ventricular infarction and an elevated inpatient mortality rate greater than 60%, thus prompting aggressive medical therapy and hemodynamic support with intra-aortic balloon counterpulsation. The initiation of therapy to reduce preload (diuretics) and afterload (nitrates, ACE inhibitors) is indicated in all patients with symptoms of heart failure; however, caution is advised if systolic blood pressure is less than 90 mm Hg or kidney dysfunction exists.

Question 29

What are complications of vascular access for a Cath?

Answer 29

Vascular access complications include hematoma, pseudoaneurysm, arteriovenous fistula, and retroperitoneal hemorrhage.

Question 30

What is the clinical presentation of a RV infarction?

Answer 30

Right ventricular infarction leads to decreased pulmonary blood flow and left atrial return, decreased preload, and impaired filling of the left ventricle. This results in the triad of hypotension, clear lung examination, and elevated jugular venous pressure.

Question 31

How is diagnosis of RV infarction made and how is it treated?

Answer 31

Diagnosis is often made clinically and can be confirmed by either ECG (leads V4R through V6R) or echocardiography (often used to exclude other causes of cardiogenic shock). Treatment consists of reperfusion, aggressive volume resuscitation, and the use of inotropes (dopamine or dobutamine) until right ventricular function improves (often 2 to 3 days after myocardial infarction).

Question 32

How is VS defect, as a complication of a STEMI diagnosed and managed? Time line after MI?

Answer 32

A ventricular septal defect is an infrequent complication of STEMI. It manifests as hemodynamic compromise in the setting of a new loud holosystolic murmur and often a palpable thrill 3 to 7 days after the initial myocardial infarction. Diagnosis is most commonly made by transthoracic echocardiography. Medical stabilization generally requires the administration of vasopressor agents and placement of an intra-aortic balloon pump. Although surgical mortality is high, inpatient mortality for patients who do not undergo surgery is nearly 100%. Percutaneous ventricular septal defect closure devices are sometimes used in nonsurgical patients, but their use is limited by anatomy and operator expertise.

Question 33

How is mitral regurg/papillary muscle rupture present after a STEMI? Timeline after MI? Diagnosis? Treatment?

Answer 33

Mitral regurgitation occurs commonly after STEMI. Mechanisms include severe left ventricular dysfunction with annulus dilatation, worsening of pre-existing mitral regurgitation, and compromise of the mitral apparatus (rupture of papillary muscle or chordae tendineae). Papillary muscle rupture often presents 3 to 7 days after initial myocardial infarction with hemodynamic compromise, pulmonary edema, and a loud systolic murmur. Diagnosis is most often made by transthoracic echocardiography, and transesophageal echocardiography may be required to plan surgical reconstruction. Treatment consists of the administration of vasodilators to reduce afterload and diuretics to decrease preload. If patients become hemodynamically compromised, the administration of vasopressors, placement of an intra-aortic balloon pump, and/or surgical intervention are required.

Question 34

When does LV free wall rupture occur? Timing? Risk factors?

Answer 34

Left ventricular free wall rupture is the most ominous mechanical complication of STEMI and has a high mortality rate. It often occurs 3 to 7 days after initial myocardial infarction. Risk factors for left ventricular rupture include advanced age, female sex, anterior myocardial infarction, and incomplete reperfusion of STEMI. Patients most commonly present with pericardial tamponade (due to hemopericardium), pulseless electrical activity, and death. Early recognition, emergent pericardiocentesis, and subsequent surgical reconstruction can improve survival.

Question 35

How is an LV thrombus detected after an MI? What is the treatment?

Answer 35

Left ventricular thrombus occurs in approximately 10% to 20% of patients after anterior myocardial infarction despite reperfusion and aggressive treatment. Transthoracic echocardiography is the most common diagnostic modality, and thrombus is detected as an echo-dense structure, often at the apex of the left ventricle ( Figure 9 ). Treatment involves the use of therapeutic warfarin for 3 to 6 months following myocardial infarction to reduce the risk of stroke or systemic embolization.

Question 36

What scoring system is used to assess the risk of death in UA and NSTEMI?

Answer 36

The TIMI risk score is the most commonly used tool for estimating the short-term risk for death and nonfatal myocardial infarction in patients with a NSTE-ACS

Question 37

How do you manage UA/NSTEMI? What’s the treatment algorithm?

Answer 37

See UA/NSTEMI

Question 38

What are other causes of ACS that are not due to plaque rupture or plaque blockage?

Answer 38

Coronary vasospasm

Takotsubo CM

Question 39

How is coronary vasospasm treated?

Answer 39

It is treated with nitrates and CCBs.