David M. Schneider, MD Clinical Professor of Family & Community Medicine, UCSF Full-Time Faculty Physician, Santa Rosa Family Medicine Residency 3/7/2017

Faculty Disclosure Nothing to disclose.

Hypertension

Public domain, via CC3.0 at http://commons.wikimedia.org/wiki/File:The_pressure_cooker.gif

HTN: Scope of the Problem—Prevalence Most common reason for office visits in non-pregnant

pts in US. ~ 30% of adults >18 y.o. 67-78 million hypertensive adults in US. Hypertension on the rise:

Obesity epidemic. Elderly (>1/2 of pts >65 – systolic or systolic + diastolic).

http://www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf; JAMA 2010;303:2043-50; Circ 2013;127:e6-e245; HTN online http://hyper.ahajournals.org/content/early/2013/11/14/HYP.0000000000000003

Prevalence – 2 African-Americans >45 y.o.:

35% of women. ~40% of men >45 y.o. Earlier onset, more severe. Less likely than Caucasians to be controlled.

European Americans >45 y.o.: 15% of women. 25% of men.

Worldwide: 1 billion.

UCLA Ctr for Health Pol Rsrch 2008; JClinHTN 2004;6:279-82; AnnFamMed 2008;6:497-502; SocSciMedicine 2007;65:1853-66

Classification of BP in Adults

•JNC-8 did not address BP classification. ASH/ISH continues prior classes (incl pre-HTN). •Goal in pre-HTN = ↓ BP to normal range, & prevent ↑ in BP, w/lifestyle modification—meds not indicated.

BP Classification SBP DBP Normal < 120 AND < 80 Prehypertension 120 – 139 OR 80 – 89 Stage 1 HTN 140 – 159 OR 90 – 99 Stage 2 HTN ≥ 160 OR ≥ 100

JNC 7—2003; ASH/ISH 2014 Public domain—Christian Heldt via http://commons.wikimedia.org/wiki/File:Magic8ball.jpg

Current BP Targets JNC-8:

<60 y.o.: <140/90. DBP: age 30-59 SOR A; 18-

29 E—Expert opinion. SBP: Expert opinion.

≥60: <150/90. (A). If ≥60 & SBP <140 & well-

tolerated cont Rx. CKD, DM: 140/90 (E).

(ASH/ISH: ≥80 y.o.: <150/90. 140/90 for everybody

else (incl 60-79). Consider <130/80 if

CKD + albuminuria.) [JNC-7:

130/80 for DM, CKD. 140/90 = everybody

else.]

JNC-8— JAMA 2013; doi: 10.1001/jama.2013.284427; ASH/ISH—JHypertens 2014;32:3-15

Target Organ Damage Heart:

CAD—angina, MI, h/o revascularization. Heart failure. LVH.

Brain: Stroke, TIA. Dementia.

Kidney: chronic kidney disease. GFR is a better indicator than serum Cr.

Eye: retinopathy. Vascular: peripheral arterial disease.

JNC 7

Diagnostic Workup of HTN – 2 Laboratory tests:

UA Hematocrit Lipid panel Blood chemistry tests:

Blood glucose Serum potassium, creatinine, and calcium

Optional (unless DM or CKD): urinary albumin/creatinine ratio.

Obtain electrocardiogram

JNC 7; 2014 ASH/ISH Guideline

Why Should We Treat HTN? ↓ BP more favorable outcomes (↓ stroke &

major CV events) – regardless of regimen (ACEI + CCB more beneficial per one study).

↓ cardiovascular events (NNT to prevent 1 death = 11; NNT = 9 if CAD or target organ damage).

DASH diet proven to ↓ CAD & stroke. In unselected population, outcomes are improved

regardless of drug regimen.

Lancet 2003;362(9395):1527-35; ArchIntMed 2008; 168:713-720; ArchIntMed 1993;153:578-81; JACC 1996;27:1214-18; Lancet 2010;375:1173; J Hypertens 2003;21(6):1055-76

JNC-8

Algorithm for Tx of HTN—1

Dx HTN

LIFESTYLE interventions— Continue through algorithm

Determine BP goal

JNC-8: JAMA 2014;311(5):507-520

Algorithm—BP Goals Determine BP goal

Age < 60; ALL DM, CKD SBP <140 DBP <90

Age ≥ 60 (NO DM or CKD

SBP <150 DBP <90

(ASH says 150/90 if ≥80, otherwise 140/90, incl 60-79)

• BP Goals: • DM OR CKD: 140/90, regardless of age. • ≥60 y.o. (ASH/ISH say ≥80): 150/90. • Everybody else: 140/90.

Algorithm—Initiating Meds CKD (w/ or w/o

DM) Everybody except CKD (incl DM)

ACEI or ARB, alone or w/other drug class

All

Thiazide or CCB, alone or combo

Thiazide, ACEI, ARB, or CCB—alone or combo

African-American NOT Afr-Am

Titration strategy: 1. Maximize 1 med before adding 2nd OR 2. Add 2nd med before max dose of 1st OR 3. Use 2 meds from different classes—2 pills or combo pill

Algorithm—Not At Goal

At Goal? Yes

• Reinforce med & lifestyle adherence. • If ready to add drug: add thiazide, ACEI or ARB, CCB—

different class, NO ACEI+ARB • If on 2 drugs, titrate both to max.

Algorithm—Still Not At Goal

At Goal?

• Reinforce med & lifestyle adherence. • ADD & titrate thiazide, ACEI or ARB, CCB (different class)

At Goal?

• Reinforce med & lifestyle adherence. • Add different class (β-blocker, aldo antagonist, other),

&/or refer to “HTN specialist”

No

No

No

Yes

Yes

Getting to Yes

At Goal?

• Continue titration/change strategy • Lather, rinse, repeat

No

• Continue current treatment & monitoring. • You’re done (finally).

JNC-8: 3(½) Simple Steps 1. Lifestyle—everybody! 2. CKD? (instead of chart of compelling indications)

a. Yes ACEI or ARB +/- other drug (B). b. No:

i. African-American: thiazide &/or CCB (B; C if DM). ii. Non-African-American: thiazide or ACEI or ARB or CCB,

alone or combo (B). 3. Increase or add.

1. Reinforce lifestyle & adherence each time.

Non-Pharmacologic Therapy for HTN Modification Recommendation ~ SBP Reduction Weight reduction Maintain Nl body wt (BMI

18.5 – 24.9) 5 – 20 mm/10kg wt loss

DASH diet Fruits, veges, lowfat dairy, low saturated & total fat

8 – 14 mm (& ↓ death)

Dietary Na restriction Max 2.4 g Na = 6 g NaCl 2 – 8 mm Physical activity Regular aerobic activity, ≥

30 min/day, most days 4 – 9 mm

Moderate ETOH (vs higher intake)

Max 2/day in men, 1/day in women or lighter persons

2 – 4 mm

JNC 7

Pharmacologic Therapy of HTN Monotherapy will control 30-50% of pts.

Majority of pts require ≥ 2 meds for control. The average hypertensive pt is on 2-3 meds (depending

on study). Vast majority of hypertensives w/diabetes will require 2

or more meds. Key points to consider:

How high is the BP? Other conditions or risk factors? Target organ damage?

http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-recommendations?source=related_link

Choosing a Medication ABCD’s:

ACE inhibitors & ARB’s. Beta blockers. Calcium channel blockers. Diuretics.

Other “forgotten” meds: Aldosterone receptor antagonists. Central sympatholytics. Alpha blockers. Direct vasodilators. Loop diuretics (better for CKD).

Diuretics (Thiazides) Usually the first choice antihypertensive agent. If pt is on a med from a different class, thiazides are

usually the top choice for the 2nd med to add. Reduce morbidity & mortality from CAD. “Virtually unsurpassed in preventing the

cardiovascular complications of HTN.” – JNC 7 Inexpensive. “Despite the various benefits of diuretics, they remain

underutilized.” – JNC 7

JNC-7; ExpOpinPharmacother 2014 Epub—doi:10.1517/14656566.2014.879118

Diuretics in CKD In pts with chronic kidney disease (CKD), use loop

diuretic if estimated GFR is below ~ 30 (thiazides less effective). Exception is metolazone (Zaroxolyn). In these pts, consider loop diuretic (furosemide,

bumetanide, torsemide, etc)

Diuretic Adverse Effects Increased electrolyte excretion:

Hypokalemia (average ↓ of 0.3-0.4 mmol/L; dietary Na restriction can minimize thiazide-induced K loss).

Hypomagnesemia. Hyponatremia.

Sexual dysfunction in men.

JAMA 2003;289(19):2560-71; JAMA 2002;288(23):2981-97

Diuretic Adverse Effects – 2 Hyperglycemia – but not contraindicated in DM.

Minimal increase in glc w/low dose thiazides (3-5 mg/dl). Proven beneficial outcomes in DM.

Hyperlipidemia Little effect at 12.5 mg HCTZ. May be temporary (< 1 yr). Proven beneficial outcomes – ↓ risk of CV events.

Hyperuricemia – ↑ gout risk, though frank gout is less common.

Hypercalcemia.

DrugSaf 2001;24:443-56; ArchIM 1999;159:551-8; JAMA 1997;277:157-66; ExpOpinPharmacother 2014 Epub—doi:10.1517/14656566.2014.879118

Commonly Used Thiazide Diuretics HCTZ 12.5 – 25 mg. Chlorthalidone 12.5 mg.

~2-3 times as strong as HCTZ (i.e., 12.5 mg chlorthalidone ≈ 25 mg HCTZ).

May have ↑ duration of action & may be more effective. Many outcomes studies done w/this drug.

Indapamide 1.25 – 5 mg. ↓ fatal stroke 39%, ↓ mortality 21%, ↓ HF 64%. 2.5 mg has ~ effect of ↓ BP as 25-50 mg HCTZ.

Thiazide Contraindications Drug allergy.

RARE crossover w/sulfa Anything else (gout, hypoK, h/o arrhythmia, etc) is a

caution, not absolute contraindication.

Negative effect on erectile function. Reduce excretion of lithium risk of toxicity.

Angiotensin Converting Enzyme Inhibitors 1st line for almost all pts.

May be less effective in African Americans & elderly, but should not be withheld.

Proven morbidity & mortality benefit in multiple clinical situations.

Use in: CHF DM 1 & 2 CAD/High risk for CAD Nephropathy

ACEI Adverse Effects Dry cough (5 – 20%). Reduced GFR (consider D/C med & w/u for RAS if

>30% ↓ in GFR or >30% ↑ in Cr). More common in renovascular HTN, CHF, polycystic

kidney disease, or CKD. Hyperkalemia (3.3 – 11%).

More common in: renal failure, DM, use of other K-sparing drug (K-sparing diuretic, NSAID), elderly.

Hypotension, dizziness, syncope. More likely in CHF, volume depletion (diuretics).

AnnIntMed 1992;117(3):234-42; ArchIM 1998;158(1):26-32; http://www.uptodate.com/contents/major-side-effects-of-angiotensin-converting-enzyme-inhibitors-and-angiotensin-ii-receptor-blockers?source=search_result&selectedTitle=1~150

Oddball ACEI Side Effects Angioedema (rare).

Swelling of lips, tongue, mouth, face. May be more common in African-Americans (2-4-

fold more common), possibly in elderly. Skin rash (a possibility with just about any med). Dysgeusia (taste disturbance) – esp captopril. Neutropenia (rarer).

Bonus effect: may reduce glc & HbA1C in DM!

AmJHTN 1993;6(5 Pt 1):337-43; AnnIntMed 1992;117(3):234-42

Angiotensin Receptor Blockers “ACE inhibitors without the cough.” Similar efficacy to ACEI’s (both are slightly less potent

antihypertensives than other agents like thiazides, CCB’s).

Similar side effect profile to ACEI’s. Lower incidence of cough (rare, but it happens).

Most pts w/ACEI-induced cough tolerate ARB’s. ~ 1/3 the (already rare) incidence of angioedema. More hypotension than ACEI’s (~2X).

NEJM 2008;358:1547-59; AnnPharmacother 2003;37:1024-7; http://www.uptodate.com/contents/major-side-effects-of-angiotensin-converting-enzyme-inhibitors-and-angiotensin-ii-receptor-blockers?source=search_result&selectedTitle=2~150

What if Creatinine Rises? Renal dysfunction associated with antihypertensive

treatment is independent of the agent used (but more common w/ACEI & ARB).

<30% ↑ in creatinine, which then stabilizes, represents a hemodynamic change, and not a structural change. Slight rise in Cr IG pressure has been reduced. ACE-I/ARB also dilate efferent arteriole, exaggerating decline

in IG pressure. If Cr ↑ > 30%, agent should be discontinued and other

causes of renal dysfunction should be evaluated (esp RAS).

NEJM 2002;347(16):1256-61

Beta Blockers Not usually a 1st choice any more unless a compelling

or other indication: Post-MI (non-intrinsic sympathomimetic) CHF CAD—control of angina Rate control in A fib No longer 1st tier in JNC-8.

EurHeartJ 2007;28:1462-536; Circulation 2008;117:2706-15; Circulation 2008;117:2691-705; http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-

recommendations?source=search_result&selectedTitle=1~150

β-Blocker Adverse Effects AV block. Bronchospasm. Increased PAD symptoms. CHF exacerbation if given in acute stage. CNS – overstated, but probably more common in

elderly. Fatigue – NNH = 57. Depression – no significant increase.

Sexual dysfunction – NNH = 199.

http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-recommendations?source=search_result&selectedTitle=1~150; http://www.uptodate.com/contents/major-side-effects-of-

beta-blockers?source=search_result&selectedTitle=1~150

β-Blocker Adverse Effects – 2 May provide inferior protection against stroke &

overall mortality, esp in smokers &/or > age 60. Atenolol may increase mortality, esp > age 60.

Impaired glc tolerance; ↑ risk of new onset diabetes. Vasodilating β-blockers like carvedilol appear OK. Effect may be temporary. Still given to post-MI diabetics.

Adverse lipid effects (labetolol may be least likely).

ß-blocker Contraindications Active bronchospasm Severe bradycardia Heart block > 1° (if no pacemaker) Pulmonary edema Hypotension with or without shock Overt heart failure should be brought under medical

control 1st Most pts w/MI d/t cocaine should not be treated with

beta blockers (risk of coronary artery spasm) http://www.uptodate.com/contents/major-side-effects-of-beta-

blockers?source=search_result&search=beta+blocker+contraindications&selectedTitle=1~150; http://www.uptodate.com/contents/use-of-beta-blockers-in-heart-failure-due-to-systolic-

dysfunction?source=search_result&search=beta+blocker+contraindications&selectedTitle=2~150

Calcium Channel Blockers (CCB) Dihydropyridines: use long acting meds.

Amlodipine Felodipine

Non-dihydropyridines: Diltiazem Verapamil

Avoid short acting dihydropyridines. Nifedipine (this is often an incorrect answer, esp if

another CCB option).

CCB Adverse Effects Edema

More likely w/DHP’s Dizziness HA (NB: Verapamil used in migraine prophylaxis.) Constipation— mostly verapamil Reflex tachycardia – DHP’s Non-DHP (verapamil, diltiazem) SE’s:

Bradycardia AV block CHF exacerbation

CCB Comparison

Drug Periph Resis

HR Conduction Contractility

DHP’s ↓↓↓ ↑ +/- +/- Diltiazem ↓↓ ↓ ↓ ↓ Verapamil ↓ ↓↓ ↓↓ ↓↓

•DHP’s more peripheral effects. •Non-DHP’s more cardiac effects.

Alpha-Adrenergic Blockers Prazosin, terazosin, doxazosin.

Orthostatic hypotension & syncope, esp 1st dose. Not usually used in initial monotherapy, except

sometimes in men w/BPH, esp if low-mod CV risk. More CV events & CHF than thiazide—but there was no

control (untreated) group. May enhance hypotensive effects of PDE-5 drugs for

erectile dysfunction (sildenafil, vardenafil, tadalafil). Tadalafil (Cialis) not recommended, or 48 h after α1 blocker. Allow 24h after last sildenafil (Viagra) or vardenafil (Levitra)

dose.

AnnIntMed 2002;137:313-20; JAMA 2000;283:1967-75

Central Sympatholytic Agents Clonidine

Dry mouth, constipation, sedation (anticholinergic). Can cause bradycardia, heart block. Rebound HTN upon withdrawal (most agents can).

Guanfacine (Tenex™) ~ clonidine w/less rash, abd pain, & milder rebound HTN.

Methyldopa Can be used in pregnancy. Rare lupus-like syndrome. Rare hemolytic anemia. Can cause hepatitis, esp in pts with liver dz.

Special Populations: Erectile Dysfunction Neutral effect on erectile function: ARBs, ACEI’s,

CCBs. Worsen erectile function: Centrally-acting α2-

agonists, β-blockers, diuretics. Contraindicated with PDE-5 inhibitors:

Nitrates (severe hypotension / circulatory collapse). α1-blockers should be used with caution; combination

may trigger hypotension. Initiate PDE-5 inhibitor at lowest dose.

Combination Therapy Preferred combinations:

ACEI or ARB + diuretic. ACEI or ARB + CCB.

Acceptable combinations: Thiazide + most others (β-blocker, CCB, K-sparing

diuretic). β-blocker + DHP CCB. [β-blocker + RAA inhibitor or adrenergic blocker]

UNacceptable combinations: 2 RAA inhibitors (ACEI, ARB, aliskiren)—dangerous.

EurHeartJ 2010;31:2205-2209; http://www.fda.gov/drugs/drugsafety/ucm300889.htm

Resistant HTN Persistent HTN despite > 3 drugs. Poor adherence most common cause. Suboptimal therapy.

Typically inadequate diuresis. Move to loop diuretic. Add spironolactone.

Med interactions. 2° HTN.

HTN 2008;51(6):1403-19; JNC 7—2003

Identifiable Causes of HTN—1 (i.e., Secondary HTN) 2 – 10% of hypertensive pts.

Chronic kidney disease (2.5 – 6%). Primary aldosteronism and other mineralocorticoid

excess states (1 – 10%). Renovascular hypertension – renal artery stenosis (0.2

– 4%). Drug induced or drug related.

Mnemonic: CARD or KARD.

JNC 7; http://emedicine.medscape.com/article/241381-overview#aw2aab6b2b3aa

Identifiable Causes of HTN—2 Endocrine

Thyroid or parathyroid disease.

Cushing’s syndrome and other glucocorticoid excess states, including chronic steroid therapy.

Pheochromocytoma (rare).

Obstructive Sleep apnea. Obstructive uropathy. Coarctation of the aorta.

Whom to Screen for 2° HTN Severe or resistant HTN (uncontrolled on 3 meds of

different classes). Malignant HTN (severe HTN + signs of end-organ

damage). An acute rise in blood pressure over a previously stable

value. Age <30 years in non-obese, non-black patients with a

confirmed negative family history of and no other risk factors (e.g., obesity) for hypertension.

Proven age of onset before puberty.

https://www.uptodate.com/contents/evaluation-of-secondary-hypertension

Additional Clues to 2° HTN Hypokalemia—aldosteronism.

Don’t just automatically assume it’s due to diuretic. ↑ Cr, abnormal UA – renal dz. Snoring, fatigue, daytime somnolence – sleep apnea.

Drug Related Causes of HTN Nonadherence Inadequate doses Inappropriate

combinations Oral contraceptives NSAID’s, COX-2 inhibitors Sympathomimetics

(decongestants, anorectics)

Cocaine, amphetamines, other illicit drugs

Adrenal steroid hormones Cyclosporine, tacrolimus Erythropoietin Licorice (including some

chewing tobacco) Some OTC supplements

and medicines (e.g., ma huang, bitter orange, ginseng, St John’s wort)

Screening Tests for 2° HTN Diagnosis Test

CKD eGFR

Coarctation of aorta CT angio

Cushing’s, glucocorticoid excess Hx, dexamethasone suppression test

Drugs Hx, drug screening

Pheochromocytoma (RARE) 24-hr urinary metanephrine and normetanephrine

Primary aldosteronism and other mineralocorticoid excess states

Plasma renin & aldosterone, ? 24-hr urinary aldosterone level

Renovascular HTN Doppler flow study, CT Angio, MRA

Sleep apnea Sleep study with O2 saturation

Thyroid/parathyroid disease TSH; PTH

JNC 7; ASH/ISH

Hypertensive Emergencies Def: acutely elevated BP with end organ damage.

Eye: retinal hemorrhages, exudates, or papilledema. Brain: hypertensive encephalopathy. Heart: angina/ischemia, HF, dissecting aortic aneurysm. Kidney: hematuria, proteinuria, ARF.

Goal: ↓ BP by 10-20% w/in 1st hr, 5-15%/next 23 hrs. Aortic dissection rapidly ↓ SBP 100-120 w/in 20 min. Stroke:

Ischemic: Tx if ≥220/120, OR ≥185/110 if tPA. Hemorrhagic: SBP 150-220 acute lowering to SBP 140 “safe.”

JNC 7; https://www.uptodate.com/contents/evaluation-and-treatment-of-hypertensive-emergencies-in-adults?source=search_result&search=hypertensive%20emergency&selectedTitle=1~150; Stroke 2015;46(7):2032-60

Treatment of HTN Emergencies Na+ nitroprusside.

Rapid action, short duration = titratable drip. Cyanide toxicity with prolonged use, esp w/renal failure. Caution w/high intracranial pressure. Continuous BP monitoring.

Nicardipine—longer half-life, harder to titrate. 1st line in acute stroke (or labetolol). Avoid in acute CHF. Caution in coronary ischemia.

Clevidipine – shorter acting, more titratable. CCB.

JNC 7; https://www.uptodate.com/contents/drugs-used-for-the-treatment-of-hypertensive-emergencies?source=see_link

Treatment of HTN Emergencies Labetolol—1st line in stroke. Safe in CAD; caution/

avoid in asthma, COPD, CHF (avoid in acute HF), bradycardia, >1° heart block.

Esmolol—ultra-short acting β-blocker. Aortic dissection.

[Fenoldopam—dopamine receptor agonist. Useful in renal failure. Contraindicated in glaucoma.

Phentolamine—catecholamine excess (pheochromocytoma).]

Lipids

http://www.publicdomainpictures.net/view-image.php?image=11891&picture=hot-dog-and-chips

Dyslipidemia Screening USPSTF (2008) recommends screening:

All men > 35 (A). Men 20-35 (B) and women > 45 (A) at increased risk for

CHD (also women 20-45 @↑ risk—B). USPSTF: fasting or non-fasting TC and HDL-C.

LDL measurement requires fasting if calculating LDL (TC - HDL - TG/5)—most panels calculate.

Direct LDL does not require fasting but is expensive. 11/16 USPSTF: did not recommend screening strategy.

2013 ACC/AHA guidelines overestimate risk for some pts.

https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/lipid-disorders-in-adults-cholesterol-dyslipidemia-screening; https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/statin-use-in-adults-preventive-medication1

2013 ACC/AHA Lipid Guidelines

“Fire & forget” instead of “treat to target.” New risk calculator.

New risk target: 10-yr ASCVD risk of 7.5% (new calculator) considered indication for Rx.

Lots of controversy.

2013 ACC/AHA Guidelines on Cholesterol –http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437738.63853.7a.citation

2013 ACC/AHA Lipid Guidelines 4 statin benefit groups:

Clinical ASCVD (atherosclerotic CV disease). LDL–C ≥190 mg/dL. 40 - 75 years of age + LDL-C 70-189 mg/dL: w/DM. No ASCVD, no DM, but w/estimated 10-year ASCVD

risk of 7.5% or higher (using new AHA calculator). No evidence for LDL targets.

2013 ACC/AHA Guidelines on Cholesterol –http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437738.63853.7a.citation

“Clinical ASCVD” ( Statin!) Per inclusion criteria for 2° prevention RCTs:

Known CAD – H/O ACS/MI, stable/unstable angina, coronary or other arterial revasc. CKD might fit in here.

Cerebrovascular dz—stroke, TIA. Peripheral arterial disease.

AAA might fit in here. DM 1 & DM2. 10-yr risk ≥7.5% on pooled cohort equation.

Step 1: ASCVD? ASCVD Statin Benefit Groups

Heart healthy lifestyle habits are the foundation of ASCVD prevention. In individuals not receiving cholesterol-lowering drug therapy,

recalculate estimated 10-y ASCVD risk every 4-6 y in individuals aged 40-75 y without clinical ASCVD or diabetes and with LDL–C 70-189

mg/dL.

Clinical ASCVD

?

Adults age >21 y and a candidate for statin

therapy

Age <75 y: High-intensity statin

(Mod-intensity statin if not candidate for high-

intensity statin)

Age >75 y OR if not candidate for

high-intensity statin: Moderate-intensity

statin

Yes

No 1.ASCVD? a) ≤75 high-intensity statin. b) >75 mod-intensity statin.

2013 AHA Cholesterol Guideline

Step 2: LDL ≥ 190? Step 3: DM?

LDL ≥190

mg/dL

High-intensity statin (Moderate-intensity

statin if not candidate for high-

intensity statin)

Moderate-intensity statin

No

DM1 or2

Age 40-75

Yes

Estimated 10-y ASCVD risk ≥7.5%*

High-intensity statin

Definitions of High- and Moderate-Intensity Statin Therapy High Daily dose lowers LDL by appox. ≥50% Moderate Daily dose lowers LDL by appox. 30% to <50%

2.LDL ≥ 190? a) High-intensity statin.

3.DM, age 40-75? a) Risk ≥7.5%high-intensity statin. b) Otherwise mod-intensity statin.

No

Step 4: ≥7.5% Risk? DM1 or2

Age 40-75

Estimate 10-y ASCVD Risk

with Pooled Cohort Equations*

Moderate-high-intensity statin

No

≥7.5% estimated

10-y ASCVD risk

and age 40-75 y

No

4.No ASCVD, LDL <190, and no DM: a) 10-yr risk

≥7.5% mod-high intensity statin.

b) Anybody else--??benefit.

Who Gets What Dose? Clinical ASCVD: High-intensity statin.

BUT if >75 Moderate-intensity statin. If not candidate for high intensity moderate-intensity

statin. LDL ≥190: High-intensity statin. DM aged 40-75:

Moderate-intensity statin. ASCVD risk ≥7.5% High-intensity statin.

All others aged 40-75 w/≥7.5% riskMod-high intensity statin.

Key Numbers Age: 40-75.

Clear benefit from statin. >75 mod-intensity statin (bene less clear).

LDL: ≥190 vs 70-189. ≥190 high-intensity statin.

7.5% risk. DM high-intensity statin. Non-DM mod-to-high intensity statin.

2013 AHA Cholesterol Guideline

Statin Doses—The New Deal No more treating to target. No more “lower is better.” New paradigm:

High-intensity statin. Moderate-intensity statin. Low-intensity statin.

Statin Doses High-intensity: ↓ LDL by

≥50%. Atorvastatin 40-80 mg. Rosuvastatin 20-40 mg.

Easy to remember.

Low-intensity: ↓ LDL by < 30%. Simvastatin 10 mg. Pravastatin 10-20 mg. Lovastatin 20 mg. Fluvastatin 20-40 mg. Pitavastatin 1 mg.

Remember: 10-20 mg of

other statins (except only 10 of simva, up to 40 of fluva).

Statin Doses—2 Everything else is moderate-intensity.

Atorvastatin 10-20. } These are the most Rosuvastatin 5-10 mg. } potent statins (esp Simvastatin 20-40 mg. } atorva/rosuva). Pravastatin 40-80 mg. -- P’s are piddling Pitavastatin 2-4 mg. -- (or pitiful). Lovastatin 40 mg. ] Fluvastatin 40 mg bid. ] Got no lov (luv) Fluvastatin XL 80 mg. ]

Secondary Dyslipidemia Per ATP III guidelines, assess for secondary

dyslipidemia before initiation of lipid-lowering therapy Diabetes mellitus Hypothyroidism Obstructive liver disease Chronic renal failure Medications (thiazide diuretics, antipsychotics)

Treatment of High LDL

STATINS!! Primary Prevention (less benefit):

↓ CAD, MI, sudden cardiac death (SCD). May ↓ total mortality.

Secondary prevention (more benefit—bang-4-$): ↓ CAD, MI, CV events. Probably ↓ total mortality. ↓ strokes.

NEJM 1995;333:1301-7; NEJM 2007;357:1477-86; JAMA 1998;279:1615-22; NEJM 2008;359:2195-2207; Lancet 2003;361:1149-58; ArchIM 1996;156:1158-72; Lancet 1994;344:1383-9; NEJM 1996;335:1001-9; Lancet 2002;360:7-22; Lancet 2003;361:1149–1158; NEJM 2004;350:1495–1504;

Circulation 2000;102:1893–1900

Statin-Related Side Effects Statin Myopathy—2/3 occur w/in 6 mo.

Myalgia (pain). Prox muscles. Myositis (elevated CK > 5-10 X ULN). <1%. Rhabdomyolysis (muscle necrosis, ↑↑↑ CK > 10X ULN,

myoglobinuria [red-brown] +/- ARF). Generally w/predisposing factors—drug interactions,

?hypothyroidism. No more statins!

>10X ULN D/C statin (& drink lots of H2O).

ArchIM 2005;165:2671-6; AmJMed 1991;91:25S-30S; ArchIM 1996;156:2085-92; BMJ. 2008;337:a2286; AmJCard 1991;68:1127-31; ArchIM 2003;163:688-92; JAMA 1990;264:71-5; ArchIM 2003;163:553-64; AmJMed 2006;119:400-9; IntJCard 2007;119:374-6

More Statin Side Effects Hepatic dysfunction:

0.4 – 3%. Consider D/C statin if ALT > 3X ULN.

Diabetes risk (RR = 1.12): High dose statins. Obesity, pre-DM @ risk. NNH = 498; however, NNT = 155. 3/2015 study: 46% ↑ DM risk/24% ↓ insulin sensitivity!

? Peripheral neuropathy.

Diabetologia 2015;58:1109-17; JHepatol 2012;56:374-80; Circ 2006;114:2788-97; EurJClinInvest 2000;30:980-7; Lancet 2002;360:7-22; BMJ 2010;340:c2197; J AMA. 2011;305:2556-64; Lancet 2010;375:735-42; NEJM 2008;359:2195-207; Circ 2004;110(Suppl I):S834; Circ 2012; 126: e282-

e284; Neurology 2002;58:1333-7; Lancet 2012;380:565-71

Liver Monitoring on Statins 2/28/12, FDA: No more routine liver

monitoring in pts on statins. LFT’s “should be performed before starting statin

therapy and as clinically indicated thereafter.” Statin-induced hepatotoxicity (esp irreversible liver

damage) is “exceptionally rare,” & likely idiosyncratic (i.e., unpredictable).

Evidence does not show that periodic LFT monitoring detects or prevents get liver dz.

ArchIM 2003;163:688-92; JFamPrac 2001;50:927-8; http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm293623.htm

Fibrate Therapy Statins are drug of choice to ↓ CV risk. Per ATP III, if triglycerides >500 mg/dL, initial

treatment should be with a fibrate to ↓ risk of pancreatitis. May also ↓ CV risk if ↑TG + ↓HDL, esp in DM). Fenofibrate ↓ CHD events, no effect on total mortality.

(FIELD trial). Fenofibrate has a lower risk of myopathy w/statins;

gemfibrozil preferred if renal dysfunction is present. Statins, niacin, or omega-3 fatty acids are all

appropriate when TG’s are ↑, but <500 mg/dl. Lancet 2005;366:1849-61; ATP 3—2002

Valvular Heart Disease

CC 3.0, Illustration from Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, via http://commons.wikimedia.org/wiki/File:2011_Heart_Valves.jpg

Switch Gears: Valvular Heart Dz Valvular heart disease generalizations:

Most valvular abnormalities give HF-like sx (DOE). Regurgitations are often treated with ACEI’s to

vasodilate & improve forward flow (“Regurgitations are relieved by RAA blockers”).

Stenoses are often best treated via surgery or procedures (“Stenoses are served by surgery”).

Almost all can lead to atrial fibrillation (less w/aortic regurg) .

Acute regurgitation can lead to cardiogenic shock.

Who Gets IE/BE Prophylaxis? Prosthetic heart valves Prosthetic material used in valve repair Prior h/o endocarditis Transplant valvulopathy Congenital heart dz:

Unrepaired cyanotic dz Repaired w/prosthetic material—for 6 mo p-procedure Repaired w/residual defects at or near prosthetic device

http://www.uptodate.com/contents/antimicrobial-prophylaxis-for-bacterial-endocarditis?source=search_result&search=endocarditis+prophylaxis&selectedTitle=1~80

Circumstances for Prophylaxis Dental procedures involving manipulation of gums or

periapical tissue, or perforation of mucosa. Incision or bx of respiratory tract mucosa (T & A,

bronch w/bx). Infected skin or musculoskeletal tissue undergoing

surgery.

NO Prophylaxis Other valve lesions. No GI or GU procedures.

Exception: established UTI w/hi risk CV condition Vaginal or Cesarean delivery.

Exception: hi risk lesion w/chorioamnionitis or pyelonephritis.

Meds for Endocarditis Prophylaxis Single dose 30 – 60 min before procedure — no more 2nd

dose! Amoxicillin 2 g

NPO: IV/IM amp (2g), cefazolin, ceftriaxone (1g). PCN allergic:

Po cephalexin 2g, clinda 600 mg, or azithro or clarithro 500 mg. IM/IV cefazolin, ceftriaxone, or clinda.

Aortic Stenosis—Key Points May be asymptomatic even with severe dz. Once sx appear, course tends to progress fairly rapidly (2-

3 yr avg survival). Classic triad: Angina, Syncope, HF (once sx appear, it

turns you to ASHes). Esp w/exertion. Exertional dyspnea is most common presenting sx (↓

exercise tolerance). Systolic ejection murmur loudest at base, rad to carotids. Atrial fibrillation, pulmonary hypertension are

preterminal findings.

AS Management Risk factor reduction.

High prevalence of CAD. Cautious treatment of HTN is appropriate.

Exercise limitations: Mild AS: competitive sports OK w/F/U. Asymptomatic mod AS: exercise testing to level of

exertion. Asymptomatic mod AS w/SVT or other complex

tachyarrhythmias: low-intensity. Severe AS: no sports.

AS Surgical Treatment Valve replacement.

Symptoms. Rarely for asymptomatic pts.

Valve replacement prolongs life and improves sx. Complications of surgery:

Stroke. Prolonged ventilation. Perioperative mortality.

Valvuloplasty may help congenital AS.

Mitral Regurgitation Trivial (“physiologic”) MR occurs in up to 70% of

adults. Etiology of pathologic MR:

Mitral valve prolapse (#1 in developed areas) Endocarditis Ischemic heart dz – MI can cause acutely Trauma Rheumatic (undeveloped nations) Congenital Drugs: cabergoline, diet pills, ergotamine

Symptoms & Signs of MR Chronic:

Asymptomatic until severe w/LV failure or AFib. DOE, ↓ exercise tolerance, fatigue (↓ CO). A fib. Higher risk of endocarditis w/severe dz.

Acute (e.g., ischemia/MI): Pulmonary edema, hypotension, cardiogenic shock.

Murmur: Holosystolic, loudest @ apex, rad to L axilla +/- back. Prolapse has midsystolic click, sl later murmur.

Management of MR Vasodilators (ACEI) – controversial in asymptomatic

pts (often recommended). Treat ischemia if present. Treat signs of CHF. Manage A fib. Consider surgery if sx.

Repair preferred for most pts (better results). Ideal to operate before EF deteriorates. MVR if extensive Ca++ of leaflet or annulus.

Supplemental Material

Hypertension

Public domain, via CC3.0 at http://commons.wikimedia.org/wiki/File:The_pressure_cooker.gif

Scope of the Problem – Control

•We’re finally making some progress. •More than half of hypertensive pts still uncontrolled. •Another study showed 44% of men & 55% of women w/HTN have adequate control.

NHANES data 1988-91 1991-94 1999-2000 2005-06 Aware of HTN 73 68.4 70 78

Treated for HTN

55 53.6 59 68

HTN controlled 29 27.4 34 43.5

ArchIntMed 2002;162(4):413-20; JAMA 2003;289(19):2560-71; AmJMed 2006;119(1):42-9; http://www.cdc.gov/nchs/data/databriefs/db03.pdf

Making the Diagnosis of HTN 2 or more “properly measured” readings at each of 2 or

more visits after an initial screen. Elevation of either SBP (>139) or DBP (>89) or both. If SBP and DBP fall into different categories, the higher

value is used. For adults who are not acutely ill and not on HTN

meds. Confirm elevated BP in contralateral arm. No caffeine, exercise, or smoking for ≥ 30 min before

measurement. Sitting quietly X ≥ 5 min, feet on floor.

AnnIntMed 2007;147:783-6; http://www.uptodate.com/contents/technique-of-blood-pressure-measurement-in-the-diagnosis-of-hypertension?source=search_result&selectedTitle=5~150

BP Changes & CV Risk In people aged 40 – 70, and from BP range 115/75 –

185/115: For every increase of 20 mm Hg in SBP, OR 10 mm Hg in

DBP, there is a doubling (2-fold) of the risk for cardiovascular disease. Pre-HTN doubles risk vs normal. Stage 1 doubles risk vs pre-HTN 4-fold > normal. Stage 2 doubles risk vs stage 1 8-fold > normal.

Treatment goal for pts w/HTN and no compelling indications: < 140/90.

JNC 7—2003

Why We Work-up HTN 3 objectives:

Assess lifestyle & identify other cardiovascular risk factors or coexisting disorders that may affect prognosis & guide treatment.

Reveal identifiable causes of HTN. Assess presence of target organ damage & cardiovascular

disease.

Conduct history and physical examination. Remember BP in both arms.

JNC 7

Mnemonic: Target Organ Damage “Heart, Brain Extremity Pain Kidneys Fail Vision wanes”

(Extremity pain PAD) Any musical genre

Mnemonic: CV Risk Factors Per JNC-7:

Age—65 F (or premature menopause), 55 M BP (HTN) Cigarettes (smoking) DM Exercise lack (physical inactivity) FH—65 F, 55 M Good cholesterol too low (HDL-C <40) High LDL-C Kidney dz (microalbuminuria, GFR < 60) Obesity (BMI > 30)

JNC 8 Part 1—Same as JNC-7!

JNC-8 BP Goals DM: 140/90. CKD: 140/90. Most people: 140/90.

>60 y.o.: 150/90. Except CKD or DM – still 140/90.

Compelling Indications—JNC-7 Compelling Indication Diu Beta-

blkr ACEI ARB CCB Ald

Ant Heart failure X X X X X Post-MI X X X High coronary dz risk X X X X Diabetes X X X X X Chronic kidney dz X X Recurrent stroke prevention

X X

JNC 7

Beta Blockers – 2 Still useful:

Resting tachycardia. LVH. Migraine. Essential tremor (non-cardioselective).

Labetolol – alpha + beta blocker Hypertensive emergencies. Pregnancy – preexisting HTN or pre-eclampsia

(unlabeled).

Common/Significant Drug Interactions With ß-Blockers Drug Effects Recommendation Amiodarone Sinus brady, AV block Extreme caution Antidiabetic agents HTN, [poss ↓ glc] Monitor Rate-sparing CCB (diltiazem, verapamil)

Brady, CHF, hypotension

Avoid (few clinical issues, however)

Digoxin Worsening bradycardia

Monitor. OK in angina + low EF (? benefit)

Epinephrine, sympathomimetics

HTN crisis Avoid if possible

Lidocaine ↑ lido level ↓ lido dose (NOT listed in ACLS protocol)

CCB Candidates African-Americans. Elderly. Angina, incl Prinzmetal’s (amlodipine, felodipine).

?↑ CV complications in DM?:

Small studies suggested ? incr MI in DM (2° outcome). Mult large studies (incl ALLHAT) found no adverse CV

effects.

NEJM 1998;338:645-52; Lancet 1998;351:1755-62; CurrHTNRes 1999;1:225-31; NEJM 1999;340:677-84; JAMA 2002;288:2981-97; AmJMed 2004;116:44-9

Direct Vasodilators Mainly for resistant HTN.

Hydralazine Can be used in pregnancy (unlabeled). ANA + lupus-like syndrome. HA, tachycardia (caution in angina/CAD). May be useful for CHF in African-Americans (unlabeled).

Minoxidil Hirsutism. Pericardial effusion. EKG changes (T wave changes common).

Special Populations: Demographic Elderly & African-Americans respond best to

thiazide diuretics or CCB’s. Less responsive to ACEI, ARB, & β-blockers—still give if

compelling indication. ACEI/ARB responsiveness improves if given diuretic. Still use β-blocker after MI.

African-Americans may respond better to Na+ restriction.

Young pts may respond better to ACEI’s & beta-blockers.

Lancet 1999;353:2008-13; BMJ 2004;328:634-40; NEJM 1993;328:914-21; AmJHTN 2001;14:241-7; JNC 7—2003

Special Populations: Diabetes HTN is common in diabetics. Diabetes and HTN ~ 2X risk of CV disease as

nondiabetics with HTN. Reduction in CV events and microvascular

complications in diabetics is seen with multiple drug classes, including: ACEIs ARBs Diuretics Ca++ channel blockers

BMJ 2000;321:412-9; BMJ 1998;317:703-13; JAMA 2002;288:2981-97

Special Populations: Diabetes—2 Calcium channel blockers:

Dihydropyridine CCBs appear inferior to ACEIs and β-blockers in reducing MI and heart failure.

Non-DCCBs (esp diltiazem) have been shown to reduce albumin excretion.

No long-term studies of the effect of α1-blockers, loop diuretics or centrally-acting α2-agonists on long-term complications of diabetes. α1-blocker arm of the ALLHAT study terminated d/t

increase in new-onset heart failure vs chlorthalidone—but NO placebo.

JAMA 2002;288:2981-97

2° HTN: “DOG & CAT PARK” Drugs Obstructive uropathy Glucocorticoid excess

Coarctation of aorta Aldosterone Thyroid/parathyroid

Pheochromocytoma Apnea (sleep) Renovascular Kidney Dz (CKD)

Clinical Clues to Renovascular HTN Acute elevation in the plasma creatinine (>30%) after

starting ACEI or ARB. Systolic-diastolic abdominal bruit that lateralizes to

one side. And more….

http://www.uptodate.com/contents/who-should-be-screened-for-renovascular-or-other-causes-of-secondary-hypertension?source=see_link; Circulation 2006;113:1474-1547

Clinical Clues to Renovascular HTN—2 Severe HTN w/4 A’s (Age, Atherosclerosis, Atrophic

kidney, Acute pulmonary edema). Onset of stage II HTN (BP ≥160/100) after age 55. Moderate to severe HTN in pts w/diffuse

atherosclerosis, esp > age 50. Moderate to severe HTN in a pt with an unexplained

atrophic kidney or asymmetry in renal sizes of >1.5 cm. Moderate to severe HTN in patients with recurrent

episodes of acute (flash) pulmonary edema or otherwise unexplained heart failure.

White-Coat HTN Up to 20-35% of HTN pts.

37-44% of resistant HTN pts. Slightly greater risk for CV events than normotensives,

less than hypertensives. High risk for developing sustained HTN. Ambulatory BP monitoring:

24-hr average BP ≥ 138/85. At equivalent office BP, those w/higher ABP have higher

risk.

HTN 2011;57:898-902; AmJHTN 2005;18:1534-40; HTN 1998;31:712-8; JHTN 2012;6:1211-6; AmJHTN 2005;18:1422-8; BPMonit 1999;4:333-41; NEJM 2003;348:2407-15; AmJHTN 2011;24:52-8; JACC 2005;46:508-15; HTN 1998;31:57-63; JHTN 1996;14:327-32

Lipids

http://www.publicdomainpictures.net/view-image.php?image=11891&picture=hot-dog-and-chips

ATP III Basics Elevated LDL-C level is a major cause of

CAD. LDL-C is the primary target for lipid-

lowering therapy. Non-HDL-C is a secondary target for lipid-

lowering therapy. Therapeutic lifestyle change is an “essential

modality in clinical management,” at all degrees of risk.

CAD Risk Factors Per NCEP ATP-III:

Age: male 45, female 55 or premature menopause w/o E replacement therapy

BP—HTN (>140/90 mmHg, or on med) Cigarette smoking (w/in 1 mo per ATP 3) Good cholesterol low—HDL <40 mg/dL Family Hx premature coronary heart disease: definite MI

or sudden death before 55 in male 1° relative, before 65 in female 1° relative

LDL is implicit—circular reasoning

ATP 3, 2002; http://www.uptodate.com/contents/atp-iii-guidelines-for-treatment-of-high-blood-cholesterol?source=search_result&search=atp+3&selectedTitle=1~71

© David M. Schneider

ATP III—HDL-C: The Good Cholesterol In both JNC-7 & NCEP ATP III, HDL-C >60 is a

negative risk factor – removes 1 point.

ATP III—CAD Equivalents

DM

Symptomatic carotid artery dz AAA Peripheral arterial dz

10-yr risk of 1st event >20% (Framingham). (probably CKD—not in ATP III yet)

Statin-Related Muscle Complaints

Lovastatin, simvastatin and atorvastatin are primarily metabolized by CYP 3A4. More interactions, more myotoxic.

Pravastatin, fluvastatin, pitavastatin and rosuvastatin – minimal 3A4 metabolism. Fewer interactions, less myotoxic.

Combination therapy: Ezetimibe NO ↑ risk of myopathy. Fenofibrate less risk of myopathy in combo

w/statins (vs gemfibrozil). Routine CK monitoring NOT recommended.

Prevention of Statin Myopathy CoQ10 100 – 200 mg daily:

No convincing evidence. Probably doesn’t hurt, may heop in 2 studies.

Vitamin D: No conclusive or convincing evidence. Probably doesn’t hurt (except high dose D in high

risk pts). Alternate day dosing.

Twice the dose every other day. Similar LDL results, no outcome data.

AmJHlthSysPharm 2004;61:515-9; AmJCard 2007;99:1409-12; AmJCard 2007 Nov;100:1400-3; AmJCard 2012;110:526-9; JACC 2007;49:2231-7; Atherosclerosis 2007;195:e182-9; TranslRes 2009;153:11-9; Atherosclerosis 2011;215:23-9; AmHtJ. 2002;144:674-7; J CVPharmacolTher

2003;8:123-6; AnnPharmacother. 2006;40:1917-23; AnnPharmacother. 2008;42:341-6; AmJCardio 2009;103:393-4

Common 3A4 Inhibitors 3 A’s:

Amiodarone Antidepressants (fluoxetine, fluvoxamine, sertraline) Antifungals (azoles)

4 others: Macrolides (esp erythro + clarithro) Non-DHP CCB’s: diltiazem, verapamil Cyclosporine (transplant pts) PI’s – inhibit everything til proven otherwise

(+grapefruit juice > 200 ml or 1 grapefruit/day!)

www.uptodate.com © David M. Schneider

Niacin in Patients with Low HDL Receiving Intensive Statin Therapy – AIM-HIGH

Conclusion: Among patients with atherosclerotic cardiovascular

disease (2° prevention) and LDL cholesterol levels of less than 70 mg/dL, there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels.

NEJM 2011;365:2255-67

Omega-3 Fats and Sudden Death

AHA guidelines suggest omega-3 supplements: Preexisting disease High risk of disease High triglycerides

GISSI found 850mg of EPA and DHA daily decreased: Mortality Nonfatal MI Stroke Rate of sudden death

ATP III—LDL Goals 0 – 1 risk factors: LDL < 160 2 risk factors: <130, OPTION of <100 CAD or CAD equivalent: <100, OPTION of <70, esp

for “very high risk pts”

Non-HDL goal = LDL goal + 30

KNOW THIS SLIDE (for ATP-III)

ATP III—Very High-Risk Patients LDL-C goal ≤70 mg/dL

Hx of MI CAD + other high risk conditions

Diabetes Metabolic syndrome Continued ischemic pain despite optimal therapy

Multiple risk factors (esp DM) Severe/poorly controlled risk factors (esp smoking)

Valvular Heart Disease

CC 3.0, Illustration from Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, via http://commons.wikimedia.org/wiki/File:2011_Heart_Valves.jpg

Aortic Regurgitation (Insufficiency) Etiology:

Congenital bicuspid aortic valve (#1 in US). Rheumatic (#1 in world). Aortic root dilation.

Marfan’s. Syphilis . Dissection .

More common with advancing age.

Aortic Insufficiency—Clinical Chronic:

Long asymptomatic period. Progressive exertional dyspnea, CHF. Pounding heart, palpitations (worse when supine or on

L side—heart vs chest wall). Acute (e.g., ischemia/MI): cardiogenic shock. Exam findings:

Wide pulse pressure. Water-hammer pulse (↑ stroke vol rapid pressure fall

d/t regurg). Blowing, decrescendo, early diastolic murmur.

Management of AI Vasodilators (nifedipine, ACEI) slow progression of AI

and reduce risk of CHF. Use in symptomatic pts. May help asymptomatic.

Avoid ß-blockers – ↓rate long diastole, may worsen regurg.

Activity limitations based on severity of AI + LV diameter.

Consider surgery (AVR) if symptomatic, increasing LV dilation, worsening LV function.

Mitral Stenosis Usually rheumatic. Sx begin in 30’s.

SOB, DOE. Pulmonary edema assoc w/exertion, fever, anemia. Occasional hemoptysis (unique among valvular dz). PE may occur.

Endocarditis rare.

MS Exam Loud S1. Opening snap. Diastolic rumbling murmur @ apex. R sided CHF signs occur later. Atrial Fib + Diastolic Murmur consider MS (A fib =

a complication of MS).

MS Management Treat CHF. Percutaneous balloon valvuloplasty.

Uncomplicated MS, limited valve Ca++. Contraindicated in severe MS, LA thrombus.

Surgical valvotomy—good results. Valve replacement.

Moderate – severe disease + CHF. Not candidate for valvotomy.