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MSPA- Cardiology > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

What is angina ?

A

Chest pain

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2
Q

What is stable angina ?

A

CP that occurs with exertion & relieved w/rest. It can also be provoked by emotional stress or exposure to cold.
Or relieved with removal of stressful stimuli or use of GTN.

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3
Q

What is the pathogenic mechanism of unstable angina?

A

It is caused by an intracoronary platelet-rich thrombus on a eroded atherosclerotic plaque leading to partial coronary occlusion.

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4
Q

What is Accelerating angina?

A

It is an exercise or stress triggered rapidly worsening chest pain.

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5
Q

What is the definition of Myocardial infarction?

A

Myocardial necrosis due to myocardial ischemia causing reduction in cardiac function, increase in cardiac biomarkers and inducing pathological Q waves in ECG.

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6
Q

What is STEMI ?

A

MI with STE + raised cardiac biomarkers and Pathological Q waves.

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7
Q

What is NSTEMI ?

A

NSTE with increased cardiac biomarkers +/- pathologic Q waves.

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8
Q

What is the pathophysiology of atherosclerotic plaque formation ?

A

Initial stage- Endothelial dysfunction and inflammation causing macrophage mediated foam cell formation.
Fatty streak formation- due to intracellular lipid accumulation.
Intermediate lesion- At this stage there is intracellular and extracellular lipid pools.
The final stage- Atheroma formation which progress to calcified fibroatherma and will eventually become a complicated lesion capable of causing turbulent flow, ischemia, vessel wall injury and thrombosis due to plaque rupture.

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9
Q

What are the risk factors for IHD ?

A
  • Age
  • Male sex
  • Family history
  • Personal hx of
    vascular disease– CVA, TIA, PAD
  • Genetics
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10
Q

What are the modifiable risk factors for IHD ?

A
  • HTN, High cholesterol and Diabetes
  • Smoking, Obesity and Sedentary
  • Raised CRP and Homocysteinaemia
  • Heavy alcohol consumption
  • Medications: OCP, COX-2 inhibitors,
    nucleoside analogues
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11
Q

What is the CVD risk classification based on family Hx ?

A
  • Average risk = No family Hx or only one secondary relative is affected.
  • Moderate risk= One first degree relative with disease onset at an avg age or two affected kins in the same side of the family.
  • High risk = Premature disease in a 1st degree kin./ 2 or more first degree kins affected./ moderate risk on both sides of the family.
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12
Q

What are the Lipid & lipoprotein abnormalities that are associated with increased risk of CHD?

A

–Elevated total and LDL cholesterol
– Low HDL cholesterol
– Hypertriglyceridaemia
– Increased non-HDL cholesterol
– Increased Lp(a)
– Increased apolipoprotein C-III
– Small, dense LDL particles
– Certain genotypes of apolipoprotein E

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13
Q

What are the risk factors for CVD ?

A
  • Diabetes and related metabolic derangements.
  • Obesity
  • Smoking- The incidence of MI is increased 6x in women
    and 3x in men who smoke at least 20 cigarettes per day.
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14
Q

What is the clinical presentation of Angina ?

A
  1. Location – substernal, epigastrium, lower jaw, teeth, between
    shoulder blades, upper extremities
  2. Character – pressure, tightness, or heaviness; strangling,
    constricting, or burning
  3. Duration – brief (≤ 10 min) but not too brief as CP that lasts “seconds” is not likely cardiac in origin.
  4. Relationship to exertion – symptoms appear or worsen with increased levels of exertion.
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15
Q

How to classify angina based on symptoms to typical, atypical and non anginal CP ?

A

The criteria
* Constricting discomfort in the chest, jaw, neck shoulder or hand.
* Precipitated by exertion
* Relived by rest or NTG within 5 min.
Typical angina- Must meet all the criteria
Atypical angina- should meet at least 2 of the criteria
Non-anginal- Meets only one or none.

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16
Q

What is the Canadian Cardiovascular society grading of angina based on symptom severity ?

A
  • Grade 01 - Angina only with strenuous exercise.
  • Grade 02- Angina with moderate exertion.
  • Grade 03- Angina with mild exertion.
  • Grade 04- Angina at rest
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17
Q

What should be the focus of physical examination in Angina ?

A
  • There are no specific physical examination findings for angina
  • Look for signs of CVD.
  • Auscultate the base to see if there is systolic crescendo-decrescendo murmur radiating to the carotid as it indicates Aortic stenosis.
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18
Q

What are the diagnostic lab studies in Angina ?

A
  • FBC- Anemia exacerbating CHD, WBC elevation if recent MI.
  • Lipid profile
  • Creatinine & eGFR
  • TFT to rule out CP secondary to hypothyroidism.
  • Ankle brachial index - To rule out PAD.
  • If angina at rest Troponin levels.
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19
Q

What are the ECG findings in angina?

A
  • None for stable angina.
  • Periods of active ischaemia will
    show ST depression &/or T
    wave inversion.
  • Tachyarrhythmias can worsen
    myocardial ischaemia.
  • Look for evidence of prior MIs,
    like pathologic Q waves or Lt
    BBB.
20
Q

What are the Echocardiography findings in Angina ?

A
  • Regional wall motion
    abnormalities due to ischemia or prior MI.
  • Low stroke volume &/or low
    ejection fraction (EF) due to HF.
  • Evidence of valve disease or aortic stenosis causing CP.
21
Q

What are the CXR findings in angina?

A
  • Not always necessary
  • Evidence of LVH
    – Ex. Enlarged cardiac silhouette
  • Evidence of HF
    – Ex. Pulmonary congestion
  • Evidence of pulmonary disease
    that could exacerbate
    underlying ischaemia
    – Ex. Emphysema/COPD
22
Q

What is the value of pre-test probability in diagnostic test choice making ?

A
  • Intermediate likelihood increases the value to diagnostic testing.
  • When the likelihood is high, a negative test can seldom rule out
    the presence of obstructive CAD because negative predictive value is low.
  • When the likelihood is low increased risk of false positive results due to low positive predictive value.
  • Hence at the extremes of probability deem the patients as having IHD or no having IHD respectively.
23
Q

What are the pre- test probability based test choices in IHD work up

A

*Very low probability - No test
*Low to moderate probability- Coronary CTA with contrast.
* Intermediate to very high probability- Invasive angiography with instantaneous wave-free ratio (iFR) and fractional flow reserve (FFR).

24
Q

What is Coronary CTA ?

A

It is a non invasive anatomical evaluation of the coronary arteries to rule out stenosis. If there is 50 to 90% stenosis invasive coronary angiogrpahy will have to be done.

25
Q

What are the provocative work-ups for coronary ischemia?

A
  • Exercise testing with ECG
  • Pharmacological provocation using dobutamine, adenosine, etc.
  • Stress CMR and stress ECHO to detect wall motion abnormalities.
  • Perfusion studies such as SPECT, PET, Contrast ECHO and Contast MRA.
26
Q

What is invasive coronary angiography and how is it done?

A

It is done in patients in whom non-invasive testing suggest high risk or it is inconclusive in the context of clinical indication. It consist of coronary angiography + Functional assessment with fractional flow reserve.

27
Q

What are the elements of standard anti-Ischemic drug therapy?

A

1st step- BB or CCB
2nd step- BB+ DHP-CCB
3rd step- add second line drugs

28
Q

What are the elements of anti-Ischemic drug therapy in high HR ( >80 BPM )?

A

1st step- BB or Non-DHP CCB
2nd step- BB+ CCB
3rd step- BB+ Ivabradine.

29
Q

What are the elements of anti-Ischemic drug therapy in low HR ( >50 BPM )?

A

1st step- DHP CCB
2nd step- Switch to long acting nitrate.
3rd step- DHP- CCB + LAN
4th step- Add nicronadil, Ranolazine, Trimetazidine.

30
Q

What are the elements of anti-Ischemic drug therapy in LV dysfunction or heart failure?

A

1st step- BB
2nd step- BB + LAN / Ivabradine.
3rd step- Add another second line drug.

31
Q

What are the elements of anti-Ischemic drug therapy in Low BP?

A

1st step- Low dose BB or Low dose non DHB-CCB.
2nd step- switch to Ivabradine/ Ranolazine/ Trimetazidine.
3rd step- combine two second line drugs.

32
Q

What is the pharmacological therapy in patients who have chronic coronary syndrome (CCS)and in sinus rhythm ?

A
  • Aspirin 75-100 mg daily in patients with previous MI or revascularization or clopidogrel 75mg daily, if aspirin intolerant.
  • Clopidogrel 75mg daily in patients with PAD, Stroke or TIA
  • Aspirin 75 to 100 mg in patients with no history clinical events but imaging evidence of coronary artery disease.
33
Q

What is the medical management of pos-PCI and post-CABG patients ?

A

– Aspirin
– Clopidogrel (Plavix)
– ACEi or ARB
– B-blocker
– Statin

34
Q

What is Prinzmetal angina?

A

Prinzmetal angina (vasospastic angina or variant angina) is a known clinical condition characterized by chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates. These symptoms occur due to abnormal coronary artery spasm. The spasm is due to either NO deficiency or pathological parasymatheticaly mediated vasospsam.

35
Q

What are the risk factors for Prinzmetal angina?

A

– Smoking
– Cocaine use
– Hyperventilation
– Provocative agents (acetylcholine, ergonovine, histamine, serotonin)

36
Q

What is the clinical presentation of Prinzmetal angina

A
  • Angina during rest.
  • Circadian pattern as sx frequently occur in the early morning hours.
  • Responds readily to GTN.
    *Pts often have underlying atherosclerotic heart disease
37
Q

What is the acute management of Prinzmetal angina ?

A
  • Monitor for continued spasm
    • Serial troponins
  • Telemetry and frequent 12-lead ECGs
  • Start ACS Tx until ruling out significant atherosclerosis.
    Aspirin +/- P2Y12 inhibitor
    – Statins
    – Heparin +/- Integrilin
  • AVOID nonselective β-blocker as May result in unopposed alpha receptor-mediated coronary vasoconstriction.
38
Q

What are the non-selective beta blockers?

A

propranolol, timolol

39
Q

What are selective beta 1 blockers ?

A

Metoprolol, atenolol, bisoprolol, nebivolol

40
Q

What is the chronic management of Prinzmetal angina ?

A
  • Eliminate any provocative stimuli (e.g., smoking, cocaine)
  • Calcium channel blockers
    – Nifedipine
    – Amlodipine (long half life)
    – Verapamil
    – Diltiazem
  • Long-acting nitrates
    – Isosorbide dinitrate
    – Isosorbide mononitrate
41
Q

What is TAKOTSUBO CARDIOMYOPATHY?

A

Transient systolic dysfunction of apical and/or mid segments of the LV causing Ballooning of the apex during systole. It is driven by catecholamine excess causing microvascular spasms. It is seen in Postmenopausal women
and triggered by intense emotional or physical stress.

42
Q

What are the findings in Takotsubo cardiomyopathy?

A
  • Chest pain, ST elevation, elevated troponin
  • Coronary angiography reveals no evidence of
    significant coronary stenosis
43
Q

What is the Tx and prognosis of Takotsubo cardiomyopathy?

A
  • Supportive therapy – IV hydration, treat complications,
    emotional support
  • Recovery of normal LV function in 4-6 weeks
44
Q

What is cocaine induced MI?

A

It is seen in young patient without risk of CVD with non-traumatic chest pain within 12 hrs of cocaine use due to Coronary artery vascoconstriction. Troponin T is elevated due to MI.

45
Q

What is the management of cocaine induced MI?

A

– Morphine, oxygen, nitroglycerin and aspirin (MONA)
– May require IV GTN
– May require benzodiazapines
– +/- Verapamil – coronary vasodilation
– Can add phentolamine (alpha-adrenergic antagonist)
– Can add labetalol (alpha and beta blocker) – reduces BP but does not affect vasospasm; avoid other beta-blockers.

MSPA- Cardiology (8 decks)

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