Modue 11 Data - Stable Ischemic Heart Disease Flashcards
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
-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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