Modue 11 Data - Stable Ischemic Heart Disease Flashcards
(103 cards)
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Angina - Recurring chest pain (CP) or discomfort occurring when a part of the heart doesn’t receive enough blood (ischemia)
* In the presence of a fixed atherosclerotic plaque when the patient is at rest…Vessels are dilated to provide adequate oxygen and blood supply to the heart.
* In the presence of a fixed atherosclerotic plaque with increased MVO2…Vessels are already maximally dilated and can provide no additional ‘supply’ , thus Angina results
* Symptoms Precipitated by exertion, cold, walking after a meal, emotional upset, fright, anger, coitus
* Relieved by rest or SL nitroglycerin (NTG)
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- Characteristic symptoms associated with “typical” chest pain
o Squeezing, heaviness, crushing or tightness , Numbness or burning, Lasts about 5-10 min.(< 20 minutes), May radiate to shoulder or arm (L > R), neck, back or abdomen
o “atypical” chest pain is more Common in women, elderly or diabetics and may be associated with symptoms termed “anginal equivalents” : Indigestion – weakness – back pain - dizziness
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Prinzmetal’s Angina (aka Variant Angina) - Vasospasm at the coronary arteries
* At rest
* Early morning hours
* Not precipitated by exertion or emotions and not relieved by rest
* Usually younger women
* +/- cardiac risk factors
Note: the differences in risk factors, presentation and treatment
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Therapeutics of SIHD:
A = aspirin, ACEI and antianginal therapy
B = β Blocker, BP and BPM (blood pressure & beats per minute (heart rate))
C = cigarette smoking and cholesterol
D = diet and diabetes
E = education and exercise
* Although not all patients have DM or smoke, it is an easy way to remember the primary areas to be addressed, as applicable, in all patients with CHD
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Primary prevention (What can be done to prevent IHD and angina) - Risk factor reduction
* Address modifiable risk factors such as BP , DM (ACE/ACCE), smoking, EToH, Meds, weight, etc…
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- An Association between elevated homocysteine levels and increased IHD events have been demonstrated.
o Lowering these levels (with folic acid, B6, B12) not been found to benefit CV events - CRP - Marker of inflammation shown to predict MI, stroke, PVD, and sudden cardiac death (ACS).
o Unspecific, Can be elevated with other conditions
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-Antiplatelets -
* Efficacy: 31% reduction in vascular events in high-risk individuals
* ASA 81-162mg or clopidogrel if ASA intolerant
o The 2012 American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis guideline on the Primary and secondary prevention of cardiovascular disease makes a recommendation for the consideration of low-dose ASA (as opposed to no aspirin) for primary prevention in all persons 40-70 years of age in the absence of bleeding risks
Some controversy exists about ASA use in primary prevention
Antiplatelets vs Control
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-Statins
* Class I
¢Lifestyle modification including weight management and physical activity are strongly recommended
¢Dietary therapy for all patients should include reduced intake of saturated fats (<7% of total calories), trans-fats (<1% of total calories) and cholesterol (< 200mg per day)
* If LDL-C ≥ 190mg/dl, evaluate for secondary causes.
o o If primary, screen family for familial hypercholesterolemia
o o Evaluate for conditions that may influence statin safety
o o High intensity statin therapy if no CIs, drug-drug interactions or history of statin intolerance
- If 10 yr ASCVD risk ≥7.5%
o o Evaluate for conditions that may influence statin safety
o o Moderate to High intensity statin therapy if no CIs, drug-drug interactions or history of statin intolerance
o o May consider moderate intensity if 10 yr ASCVD risk > 5% - And of course, if the patient was diabetic, that would also be an indication for a statin independent of other possible indications. Please refer back to the endocrine discussions
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ACEIs (ARBs) -
ACE inhibitors should also be considered in patients at high risk for developing SIHD. Considerable evidence has now been amassed in support of the concept that the RAAS is a risk factor for vascular disease, independent of other cardiovascular risk factors. These studies, both experimental and clinical, suggest that patients at risk for end events can benefit from inhibition of the RAS system
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Secondary Prevention (What can be done in those currently with SIHD and to prevent secondary CV events)
* Address modifiable risk factors such as BP (JNC8 & ACC/AHA), DM (ACE/ACCE), smoking, EToH, Meds, weight, etc…
o See above PLUS some additions modification
* ACEIs (ARBs as an alternative) - ACEI have not been found to improve symptomatic angina, BUT
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o Significant reduction in cardiovascular death, MI and stroke with a minimal reduction in BP (p <0.001)
o In the setting of ASCVD, ACEIs stabilize coronary plaques, provide for restoration and / or improvement in endothelial function, inhibit vascular smooth muscle growth and possible prevent oxidative stress
o ACC/AHA recommendation
ACEI should be used in high risk patients (and no LV dysfunction) with IHD
ACEI should be given to all patients with IHD with prior MI, HTN, DM, CKD and/or systolic dysfunction (LVEF < 40%)
ACEI may be considered in low risk patients with IHD with mildly reduced or normal EF in whom CV risk factors are well controlled and revascularization has been performed
ACEI inhibitors may be considered in patients with stable ischemic heart disease and other vascular disease
»this basically includes all patients with SIHD
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- Antiplatelets
o - The 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease recommends Treatment with aspirin 75 to 162 mg daily should be continued indefinitely in the absence of contraindications in patients with SIHD, CHD (and equivalent conditions (eg Diabetes))
ASA 81-162mg or clopidogrel if ASA intolerant
Patients who have a gastrointestinal bleed on low-dose aspirin should, after the episode is controlled, be treated with aspirin (81 mg/day) plus a proton pump inhibitor.
have not been found to improve symptomatic angina, but still indicated for cardiovascular benefits provided
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- Statins -
o SIHD Is considered clinical ASCVD. As we will see (next week), patients with clinical ASCVD (Acute coronary syndromes , A history of myocardial infarction , Stable or unstable angina , Coronary or other arterial revascularization , Stroke, Transient ischemic attack or Peripheral arterial disease presumed to be of atherosclerotic origin) should be given a HIGH Intensity statin (or moderate intensity if not a candidate for high intensity) therapy in the absence of contraindications or documented adverse effects. This is Regardless of baseline LDL
You MUST know those agents and doses which constitute moderate and high intensity
has not been found to improve symptomatic angina, but still indicated
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Prinzmetal’s angina- Statins have been shown to be effective in preventing coronary spasm and may exert their benefits via endothelial nitric oxide or direct effects on the vascular smooth muscle.
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- “Other” Lipid Lowering Therapies
o For patients with clinical ASCVD who are on high intensity statin and do not achieve a 50% reduction in LDL-C (Or LDL-C > 100mg/dl), additional therapies should be considered
o 2016/2017 ACC Expert Consensus Decision Pathway (ECDP) on the Role of Non-statin Therapies for cholesterol lowering
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Hypertension with SIHD
- In adults with SIHD and hypertension, a BP target of less than 130/80 mm Hg is recommended.
- Initial agents
¢β – Blocker (BP reduction & SIHD symptom reduction)
¢ACEIs / ARBs (BP reduction & CV risk reduction) - GDMT beta blockers for BP control or relief of angina include carvedilol, metoprolol tartrate, metoprolol succinate, nadolol, bisoprolol, propranolol, and timolol.
o atenolol should not be used because it is less effective than placebo in reducing cardiovascular events
o Avoid beta blockers with intrinsic sympathomimetic activity. - Add on therapies for persistent HTN
¢Patients with anginal symptoms – add dihydropyridine calcium channel blocker (CCB)
¢Patients whose angina symptoms are controlled - addition of dihydropyridine CCBs, thiazide diuretics, and/or mineralocorticoid receptor antagonists (MRAs) may all be considered.
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Diabetes with SIHD
* In patients with SIHD, ACC/AHA recommends a target A1C < 7% for most patients, but a more lenient goal of < 8% for frail or high risk patients (long duration, short life expectancy, risk of hypoglycemia, etc)
* Metformin is the drug of 1st choice for those with DMII and SIHD (unless contraindicated). Recent trial have demonstrated newer therapies for DMII that significantly reduce CV events and should be used as ADD ON THERAPY with metformin in those with DMII and ASCVD whose glucose remains uncontrolled
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Pharmacotherapy for prevention of anginal symptoms (ie. reduce the frequency of symptoms / improve exercise capicity).
* These medications as a whole either increase oxygen supply or decrease MVO2
* There is no evidence that any of these agents prevent ACS or improve survival in patients with SIHD.
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-Beta blockers - Decrease HR, contractility and wall tension
* ACC/AHA recommendation - Initial treatment in all patients with chronic stable angina unless CI
o o Beta 1 selective agents Preferred in patients with COPD, PVD, DM, dyslipidemia, and sexual dysfunction (atenolol, metoprolol)
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o o If LVD (EF ≤40%) due to HF or s/p MI, use one of carvedilol, metoprolol succinate, or bisoprolol
§ DONT FORGET ABOUT OUR HF DISCUSSIONS. Only 3 BBs are approved in LV dysfunction
If patient is not on approved BB, gradually taper off the old and start the new via a taper
* o Avoid agents with ISA (eg pindolol)
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* Goal resting HR = 55-60 bpm (unless symptomatic, i.e. Light headed, dz, syncope)
* Goal exertional HR = 100 bpm or less; Not greater than 20 bpm or 10% increase over resting HR
o § Therapy should be optimized (dose increased) (NOTE RESTING HEART RATE GOALS ABOVE) prior to adding agents or changing to alternative agent... if possible
o ADRs - bardaycardia, hypotension, fatigue, sexual dysfunction, bronchospasm (non-selective agents)
o CIs - baseline bradycardia (HR< 50-60), hypotension, 2nd / 3rd degree heart block, decompensated HF, reactive airway disease (non-selective agents only)
* Do not use in vasospastic (Prinzmetals) angina - Worsens and prolongs episodes because of unopposed alpha stimulation \ vasoconstriction
BBs
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-Beta blockers - Decrease HR, contractility and wall tension
* ACC/AHA recommendation - Initial treatment in all patients with chronic stable angina unless CI
o o Beta 1 selective agents Preferred in patients with COPD, PVD, DM, dyslipidemia, and sexual dysfunction (atenolol, metoprolol)
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o o If LVD (EF ≤40%) due to HF or s/p MI, use one of carvedilol, metoprolol succinate, or bisoprolol
§ DONT FORGET ABOUT OUR HF DISCUSSIONS. Only 3 BBs are approved in LV dysfunction
If patient is not on approved BB, gradually taper off the old and start the new via a taper
* o Avoid agents with ISA (eg pindolol)
* Goal resting HR = 55-60 bpm (unless symptomatic, i.e. Light headed, dz, syncope)
* Goal exertional HR = 100 bpm or less; Not greater than 20 bpm or 10% increase over resting HR
o § Therapy should be optimized (dose increased) (NOTE RESTING HEART RATE GOALS ABOVE) prior to adding agents or changing to alternative agent... if possible
o ADRs - bradycardia, hypotension, fatigue, sexual dysfunction, bronchospasm (non-selective agents)
o CIs - baseline bradycardia (HR< 50-60), hypotension, 2nd / 3rd degree heart block, decompensated HF, reactive airway disease (non-selective agents only)
* Do not use in vasospastic (Prinzmetals) angina - Worsens and prolongs episodes because of unopposed alpha stimulation \ vasoconstriction
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-Calcium Channel Blockers -
* May increase myocardial oxygen supply via a Decrease coronary vascular resistance and increase coronary blood flow
PLUS
* Non-DHPs CCBs (verapamil, diltiazem) decrease HR, contractility and wall tension (via reduction in BP)
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-Calcium Channel Blockers -
* May increase myocardial oxygen supply via a Decrease coronary vascular resistance and increase coronary blood flow
PLUS
* Non-DHPs CCBs (verapamil, diltiazem) decrease HR, contractility and wall tension (via reduction in BP)
* DHPs CCBs (amlodipine, felodipine, etc) Decrease wall tension (via reduction in BP) and Variable effect on contractility
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- CCBs are used in combination with beta blockers when initial treatment with beta blockers is not successful OR as a substitute for a beta blocker when beta blockers are contraindicated or cause side effects
- All calcium channel blockers are effective in the treatment of stable angina pectoris, the choice of a particular agent should be based on potential drug interactions and adverse events. However, short-acting, rapid onset CCBs (eg. immediate release nifedipine) are limited by reflex tachycardia which may exacerbate ischemia, thereby preventing its use as monotherapy in this disorder. Less common with long-acting or second generation dihydropyridines such as amlodipine or felodipine.
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* ACC/AHA recommendations
o Non-DHP* - First-line (initial therapy) in patients with contraindications, unsuccessful therapy or side effects with beta-blockers
Should be used with caution in patients with left ventricular systolic dysfunction or heart failure due to their negative inotropic effect. DHP CCBs would be preferred (amlodipine, felodipine) in this instance
o Non-DHP - Add-on therapy to beta-blockers with persistent symptoms
Extreme caution should be exercised when adding non-DHP to a BB due to risk of AV (heart) block. Combination should generally be avoided and a DHP CCB used
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o DHP CCB- Add-on therapy to beta-blockers with persistent symptoms if non-DHP cannot be used due to HR <50-60 bpm (bradycardia) or contraindications
Preferred over other calcium channel blockers in patients with cardiac conduction defects such as sick sinus syndrome, sinus bradycardia, or significant AV conduction disturbances
A number of studies have demonstrated the effectiveness of the dihydropyridines in stable angina with No apparent difference was seen between dihydropyridine and nondihydropyridine drugs.
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o Non-DHP - First-line in patients with variable angina or Prinzmetal’s angina
* ADRs - bradycardia (non-DNPs), hypotension, heart block, constipation (verapamil), reflex tachycardia (DHPs, but not amlodipine or felodipine),peripheral edema (DHPs)
* CIs
o Non-DHPs
§ Systolic dysfunction (eg s/p MI, HF)
§ Avoid in patients with baseline bradycardia, 2nd or 3rd degree heart block or hypotension
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DHPs
§ LV dysfunction (Except amlodipine / felodipine)
§ Older agents (eg nifedipine) have a rapid onset and can trigger reflex tachycardia... a situation that increases MVO2
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-Nitrates
* Decreases wall tension (via reduction in BP and LV volume)
* May increase HR (reflex tachycardia) and no effect on contractility
* Dilates coronary arteries i.e. ¬ coronary blood flow especially to ischemic regions
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* ACC/AHA recommendations (long acting) for nitrates
o o Add-on therapy to beta-blockers and/or CCB in patients with persistent symptoms
o Should NOT be used as monotherapy for chronic stable angina
Monotherapy with nitrates for the prevention of ischemia should generally be avoided
Reflex increases in sympathetic activity and heart rate, with resultant increases in myocardial oxygen demand, may occur secondary to nitrate-induced venodilation.
o Frequent and continuous exposure to organic nitrates leads to progressively diminished vasodilating effects i.e. tolerance develops. A nitrate-free interval during treatment (8-12 hours each day minimizes the development of tolerance, but would otherwise leave patient unprotected if used as monotherapy during that time frame
o ADRs
o Headache, flushing, postural hypotension, reflex tachycardia
o CIs - PDE5Is .. Please refer back to Men's Health
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o Cardiovascular effects (particularly hypotension and even death) have been reported with the use of PDE5Is and nitrates
o In an emergent situation, a patient who has taken sildenafil may be given a nitrate after 24 hours; for tadalafil, after 48 hours. Vardenafil does not have a suggested time interval, but blood pressure and heart rate did not change when the drug was taken 24 hours before nitrate administration.
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* SL NTG (quick acting)
o o First-line therapy with infrequent attacks (1 every few days or a few times per month) and prior to known activity that causes angina, but use more than occasionally indicates the need to address other anti-anginal therapy optimization
No benefit in terms reducing all cause mortality (LVD, SCD, etc)
o o ALL patients should have access to SL NTG or NTG spray
Nitrate tolerance does not develop with the sublingual route of administration. Use of long-acting nitrates also does not result in tolerance to the use of sublingual products.
o o Education / storage???
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* SL NTG (quick acting)
o o First-line therapy with infrequent attacks (1 every few days or a few times per month) and prior to known activity that causes angina, but use more than occasionally indicates the need to address other anti-anginal therapy optimization
No benefit in terms reducing all cause mortality (LVD, SCD, etc)
o o ALL patients should have access to SL NTG or NTG spray
Nitrate tolerance does not develop with the sublingual route of administration. Use of long-acting nitrates also does not result in tolerance to the use of sublingual products.
o o Education / storage???
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Ranolazine - Its mechanism is hemodynamically independent, leading to only minimal effects on resting and exercise heart rate and blood pressure
* FDA
o o To prevent anginal episodes in patients requiring additional therapy after beta-blockers, calcium channel blockers and nitrates
can be a substitute for beta blockers for relief of anginal symptoms if initial treatment with beta blockers leads to unacceptable side effects or is ineffective or is contraindicated.
o o To prevent anginal episodes in patients who cannot take maximum dosage of other anti-anginal therapies
can be combined with beta blockers for relief of symptoms if initial monotherapy with beta blockers is unsuccessful.
* American College of Cardiology Foundation/American Heart Association/American College ofPhysicians/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society for Cardiovascular Angiography and Interventions/Society of Thoracic Surgeons (ACCF/AHA/ACP/AATS/PCNA/SCAI/STS)
o Used as a substitute for beta blockers for relief of anginal symptoms IF initial treatment with beta blockers leads to unacceptable side effects or is ineffective or is contraindicated.
o Can be combined with beta blockers for relief of symptoms if initial monotherapy with beta blockers is unsuccessful.
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Ivabradine - Selective I(f) inhibitor which lowers heart rate and improves myocardial oxygen balance by prolonging diastole
* use of ivabradine NOT RECOMMENDED in patients with stable angina who do not have clinical heart failure
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The Older patient
* Elderly patients with coronary heart disease often present with atypical symptoms, including exertional dyspnea. Silent myocardial ischemia is also common.
* The presence of comorbid conditions and difficulties managing medications in older adults also complicate care.
o The approach to the management of angina in older adults should not differ substantially from that advocated for younger patients
o All of the drugs used in younger patients for the control of anginal symptoms are appropriate for older adults. However, older adults may experience more side effects, particularly hypotension from nitrates and calcium channel blockers and central nervous system effects from beta blockers.
o Elderly patients may need to be started on lower doses initially and should be monitored carefully for side effects.
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Prinzmetal's (vasospastic) angina - — Patients with vasospastic angina typically present with a chronic pattern of recurrent episodes of chest pain. The quality of the chest pain is indistinguishable from classical angina pectoris associated with obstructive coronary artery disease; however, the context in which it occurs differs. In particular, patients with vasospastic angina report that their episodes are predominantly at rest and that many occur from midnight to early morning. Each episode of chest pain generally lasts 5 to 15 minutes but episodes may last longer
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* Non-DHP (verapamil / diltiazem) - First-line in patients with variable angina or Prinzmetal’s angina
* DHP CCBs are an acceptable alternative to Non-DHP CCBs where decreases in rate and contractility would be problematic
* Long acting nitrates
o First-line in patients with contraindications, unsuccessful therapy or side effects with CCB
o Add-on therapy to CCB in patients with persistent symptoms
* Short acting nitrates
o To relieve acute coronary vasospasm
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* BBs - Worsens and prolongs episodes of vasospasm b/c of unopposed alpha stimulation. DO NOT USE
There may be some potential for the use of statins, the role has not yet been defined (J Am Coll Cardiol. 2008;51(18):1742. ). . Further studies are required to assess clinical outcomes before we recommend routine statin therapy in vasospastic angina patients who do not have other indications.
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There may be potential concern with high doses of aspirin, as it may inhibit prostacyclin (an intrinsic vasodilator)
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One thing we need to keep straight is terminology and what we are trying to achieve. So for example, if a patient is experiencing an acute anginal episode, a beta blocker is not what we are looking for, but rather SL NTG that a patient has been properly educated about.
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One thing we need to keep straight is terminology and what we are trying to achieve. So for example, if a patient is experiencing an acute anginal episode, a beta blocker is not what we are looking for, but rather SL NTG that a patient has been properly educated about.
* [How do I take it, when should I take it, when should I call for help,,, how should it be stored, who should it be prescibed for ?].
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If prevention is our goal (ie improve exercise tolerance, reduce frequency of acute anginal episodes), then we are looking for longer term treatment with BB, CCB and/or long acting nitrate .. in that order if possible and optimizing therapy along the way.
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lets take this patient for example .. he is otherwise healthy so to improve his QOL (exercerise tolerance, less reliance on SL NTG, etc) a beta blocker would be ideal because they
* Decrease HR, contractility and wall tension (via reduction in BP)
* There are no contraindications (Baseline bradycardia (HR < 50-60), Hypotension, 2nd or 3rd degree heart block, Sick sinus syndrome, History of reactive airway disease (esp non-selective agents), Severe PVD or Decompensated HF)
* which one should I choose?
o Beta1-selective agents Preferred in patients with COPD, PVD, DM, dyslipidemia, and sexual dysfunction (Metoprolol, atenolol)
o What if they had stable HF?
In this situation, not only will these agent help with IHD, but as we have seen last week, they are associated with improved mortality following an MI
Which beta blocker would be indicated with the comorbidity of HF?
o agents with Intrinsic sympathomimetic activity agents – should NOT be recommended (Pindolol, acebutolol) .. Why?
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What should my goal of therapy with this BB be ?
* Goal resting HR = 55-60 bpm (unless symptomatic bradycardia, ie. Light headed, dz, syncope)
o (HR < 50bpm if angina symptoms continue)
* Goal exertional HR
o Keep HR at 100 bpm or less
o Not greater than 20 bpm or 10% increase over resting HR
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Prior to adding on a second agent, am I at my goal heart rate? thus, HR becomes critical component of monitoring along with typical BB side effects.
When adding a second agent, again consider possible contraindications or co-morbidities that would prompt the use of one vs another. Again in this patient, if they were optimized on BB therapy or we were limited from increasing the dose of the BB any further (eg due to bradycardia) , options would be a CCB or long acting nitrate. which would you choose ?
* some thoughts non-DHP CCBs in combination with BB can cause AV block or worsen bradycardia
o So when should they be used ?
* older, rapid onset DHPs (eg nifidipine) are associated with reflex tachycardia (which increases MVO2). new agents with slow onset and longer duration (eg amlodipine, felodipine) are not associated with this problem
o so when should they be used ?
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Just as with BBs, what are the goals/end points of therapy with CCBs and or long acting nitrates (ie monitoring)?
* Why are long acting nitrates NEVER used as monotherapy and sticking with this class of drugs, please also consider what is meant by a "nitrate free period"?
* What is the concern with nitrates and PDE5Is (recall mens health)?
o What if there was an emergent situation and a PDE5I was used recently ?
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The term ischemic refers to a decreased supply of oxygenated blood to the heart muscle. IHD is caused by stenosis, or narrowing, in one or more of the major coronary arteries that supply blood to the heart, most commonly by atherosclerotic plaques. Atherosclerotic plaques may impede coronary blood flow to the extent that cardiac tissue distal to the coronary artery narrowing is deprived of sufficient oxygen to meet oxygen demand.
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IHD results from an imbalance between myocardial oxygen supply and oxygen demand.
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In patients without IHD, coronary blood flow increases in response to increases in myocardial oxygen demand. However, in patients with IHD, coronary blood flow cannot sufficiently increase (and may decrease) in response to increased oxygen demand, resulting in angina.
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Modifiable Risk Factors for IHD:
- cigarette smoking
- dyslipidemia
- - elevated LDL or total cholesterol
- - reduced HDL cholesterol
- diabetes mellitus
- HTN
- physical inactivity
- obesity
- low daily fruit/veg consumption
- alcohol overuse
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Nonmodifiable Risk Factors for IHD:
- Over 45 years for men
- Over 55 years for women
- Men and postmenopausal women
- family history
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Nonatherosclerotic conditions that can cause angine-like symptoms:
Cardiac conditions:
- aortic dissection
- aortic stenosis
- coronary artery vasospasm
- pericarditis
- valvular heart disease
- severe uncontrolled HTN
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Nonatherosclerotic conditions that can cause angina-like symptoms:
Noncardiac conditions:
- anemia
- anxiety disorders
- carbon monoxide poisoning
- chest wall trauma
- cocaine use
- esophageal reflux/spasm
- PUD
- pleuritis
- PNA
- pneumothorax
- pulmonary embolus
- pulmonary HTN
- thyrotoxicosis
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Pain may radiate to the neck, jaw, shoulder, back, or arm.
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The five components commonly used to characterize chest pain are: quality, location, duration, provoking factors, and mitigating factors.
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Patients typically describe chest pain as a sensation of pressure, heaviness, tightness, or squeezing in the anterior chest area. Sharp pain and pain reproducable by palpation are not typical symptoms of angina.
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Chest pain may be accompanied by dyspnea, nausea, vomiting, or diaphoresis.
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Chest pain typically persists for several minutes.
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Chest pain symptoms are often provoked by exertion (walking, climbing stairs, yardwork, housework) or emotional stress and relieved within minutes by rest or sublingual nitroglycerin. Other precipitating factors include exposure to cold temperatures and heavy meals. Pain that occurs at rest (without provocation) or that is prolonged and unrelieved by sublingual nitroglycerin is indicative of ACS.
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Some patients, most commonly women, the elderly, and patients with diabetes, may present with atypical symptoms including indigestion, gastric fullness, back pain, and SOB. Patients with diabetes and the elderly may experience associated symptoms, such as dyspnea, diaphoresis, nausea, fatigue, and dizziness, without having any of the classic angina symptoms.
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In some cases, "silent ischemia" occurs in which patients are asymptomatic
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Common clinical manifestations of IHD include chronic stable angina and the ACS of unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
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Angina pectoris, or simply angina, is the most common symptom of IHD.
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Angina is discomfort in the chest that occurs when the blood supply to the myocardium is compromised.
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Chronic stable angina is a chronic occurrence of chest discomfort due to transient myocardial ischemia with physical exertion or other conditions that increase oxygen demand.
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For the exam we are focusing on chronic stable angina.
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Primary prevention of IHD:
- co-morbid disease management
- lifestyle modification
- antiplatelet and statin therapy
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Secondary prevention of IHD:
- co-morbid disease management
- lifestyle modification
- antiplatelet and statin therapy
- ACEI and anti-anginal therapy
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Who should receive secondary prevention?
All patients with clinically significant atherosclerotic cardiovascular disease (ASCVD).
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Those patients that should receive secondary prevention:
- have clinically significant ASCVD
- hx of MI
- hx of angina
- hx of prior revascularization
- hx os stroke or TIA
- symptomatic PVD
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Note: oftentime's patients with conditions such as IHD have multiple comorbidities. So, for example, HF + IHD + HTN. Evaluation and treatment of these patients require comprehensive management. If you recall in HF, BBs have demonstrated benefits and should be part of all patients' therapy with stable disease. The caveat was that only carvedilol, metoprolol succinate, and bisoprolol are approved for us in HF. Fast forward now to the patient that also has IHD . Therapy of IHD recommends BBs as first line therapy (barring contraindications). Contemporary clinical outcomes have demonstrated superiority with carvedilol, but in general the only beta blocked that should not be used are those with IS (intrinsic sympathomimetic activity). Considering both conditions then, it would be prudent to choose a BB beneficial for both conditions (carvedilol, metoprolol succinate, bisoprolol).
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Therapeutics of IHD can be easily remembered with this mnemonic:
- A = aspirin, ACEIs, and antianginal therapy
- B = Beta-blocker and BP
- C = Cigarette smoking and cholesterol
- D = Diet and diabetes
- E = Education and exercise
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No matter what, for patients with chronic stable angina:
- aspirin
- ACEI
- BB
- statin
- SL NTG
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If patient can't tolerate BB due to low HR (without BB), start on CCB and/or Long-Acting nitrate.
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Ranolazine is added as an "add-on" if patient is still experiencing discomfort.
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If allergic to aspirin, start patient on clopidogrel instead.
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92
You can switch out an ACEI for an ARB... BUT, if the patient has angioedema you cannot give the patient any ACEI or ARBs.
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93
Monitoring: ADRs and DIs in all meds
- ACEI: kidney function, K, angioedema, cough
- ARB: kidney function, K, angioedema
- ASA: S/sx of bleeding
- BBs: HR, BP, hepatic/renal function
- Statins: LFTs, lipid panel, muscle pain
- NTG: HR, BP, O2, RR
- CCB: HR, BP, ECG, Chem-7, hepatic/renal function
- LA Nitrate: HR, BP, additive hypotension
- Ranolazine: QT, ECG, SCr, BUN, urine output (kidney function)
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94
Limitations of ACEI:
Bilateral renal artery stenosis is a contraindication for ACEI and ARBs because of the risk for overt renal failure. Patients treated with ACEI may develop a chronic cough secondary to bradykinin accumulation. Both ACEI and ARBs cause fetal injury and death and are contraindicated in pregnancy.
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95
Limitations of ARBs:
For patients who develop a persistent ACEI-induced cough. Contraindicated in bilateral renal artery stenosis and pregnancy.
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96
Limitations of ASA:
Renal failure and bleeding risk.
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97
Limitations of BBs:
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98
Limitations of BBs:
Beta blockers are considered first line therapy and should be dosed to a resting HR of 55-60 BPM. If the patient is still symptomatic at that HR, then doses cannot be increased, but rather an additional agent (usually a DHP CCB) is added. Maximum HR with exercise of 100 BPM or less or 20 BPM above the resting HR.
Beta-blockers with intrinsic sympathomimetic activity 9ISA), like acebutolol, pindolol, penbutolol, may produce lesser reductions in myocardial oxygen demand and should be avoided in patients with SIHD.
Beta blockers are CI in patients with severe bradycardia (HR<50) or atrioventricular (AV) conduction defects in the absence of a pacemaker. BBs should be used with particular caution in combination with other agents that depress AV conduction (eg, digoxin, verapmmil, diltiazem) because of the increased risk of bradycardia and heart block.
All BBs may mask the tacycardia and tremors (but not sweating) that commonly accompany episodes of hypoglycemia in diabetes. In addition, nonselective BBs may alter glucose metabolism and slow recovery from hypoglycemia in insulin-dependent diabetes.
B1-selective agents are preferred because they are less likely to prolong recovery from hypoglycemia.
Abrupt BB withdrawal may increase the frequency and severity of angina. possibly because of increased receptor sensitivity to catecholamines after long-term B-blockade. If the decision is made to stop BB therapy, the dose should be tapered over several days to weeks to avoid exacerbating angina.
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99
Limitations of statins:
Hepatic failure, drug interactions and myalgia
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100
Limitations of NTG:
Concomitant use of nitrates and PDE5Is enhances cGMP-mediated vasodilation and can result in serious hypotension, decreased coronary perfusion, and even death.
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101
Limitations of CCBs:
CCBs are recommended as alternative treatment in SIHD when BBs are CI or not tolerated. In addition, CCBs may be used in combination with BB when initial treatment is unsuccessful. A BB and a DHP CCB may improve symptoms better than either drug used alone. However, the combination of a BB with either verapamil or diltiazem should be used with extreme caution because both drugs decrease AV nodal conduction, increasing the risk for severe bradycardia or AV block when used together.
For patients with variable and unpredictable occurences of angina, indicating possible coronary vasospasm, CCBs may be more effective than BBs in preventing angina episodes.
Verapamil and diltiazem are CI in patients with bradycardia and preexisting conduction disease in the absence of a pacemaker. Because of their negative inotropic effects, CCBs may cause or exacerbate HF in patients with HFrEF and should be avoided in this population. The exceptions are amlodipine and felodipine that have less negative inotropic effects compared with other CCBs and appear to be safe in patients with left ventricular systolic dysfunction.
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102
Limitations of LA Nitrates:
See limitations of nitrates above. Also, the major limitation of nitrate therapy is the development of tolerance with continuous use.
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103
Limitations of Ranolazine:
Has minimal effects on HR or BP; thus, it may be an option in SIHD patients with low baseline BP or HR. Ranolazine is indicated as a first-line treatment for chronic stable angina. Cost is a limitation. QT prolongation and large number of drug interactions.
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