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Prevalence 33.5% in U.S. adults; >75 million affected (prevalence equal for men and women, highest in African American adults at 44%)
↑ Age → ↓ arterial compliance → systolic HTN
Essential (95%): onset 25-55 y; ⊕ FHx. Unclear mechanism but ? additive microvasc renal injury over time w/ contribution of hyperactive sympathetics (NEJM 2002;346:913). Both genetic (Nature 2011;478:103) & environmental risk factors (Na, obesity, inactivity) Blacks more likely to be salt sensitive and have less activation of renin-angiotensin system, explaining preference for thiazides & CCB over ACEI or ARB
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(2) reveal 2° causes of hypertension; (3) assess for target-organ damage
History: CAD, HF, TIA/CVA, PAD, DM, renal insufficiency, sleep apnea, preeclampsia; ⊕ FHx for HTN; diet, Na intake, smoking, alcohol, prescription and OTC meds, OCP
Physical exam: [check mark] BP in both arms; funduscopic exam; BMI & waist circumference; cardiac (LVH, murmurs) including signs of HF, vascular (bruits, radial-femoral delay); abdominal (masses or bruits); neuro exam
Testing: K, BUN, Cr, Ca, glc, Hct, U/A, lipids, TSH, urinary albumin:creatinine (if ↑ Cr, DM, or peripheral edema), ? renin, ECG (for LVH), CXR, TTE (eval for valve abnl, LVH)
Ambulatory BP monitoring (ABPM): predictive of CV risk and ↑ Se & Sp for dx of HTN vs office BP (HTN 2005;46:156). Consider for suspected episodic or white coat HTN, resistant HTN, HoTN sx on meds, or suspected autonomic dysfxn. Rec by some guidelines to confirm HTN dx, so utilization may expand (BMJ 2011;342:d3621 & 343:d4891).
Goal: in general, <140/90 mmHg
In elderly: data sparser, but benefit, albeit w/ less strict BP target (NEJM 2008;358:1887); thus, consider <150/90 mmHg if either (a) ≥80 y and w/o DM or CKD (ASH/ISH rec), or (b) ≥60 y (but no need to downtitrate if <140/90 & tolerating meds) (JNC 8 rec)
In Pts w/ DM and/or CKD: prior targets of <130/80 not supported by data (and harm if target <120; NEJM 2010;362:1575), but may consider if CKD & albuminuria for renal protection (ASH/ISH rec based on NEJM 1994;330:877)
Lifestyle modifications (each ↓ SBP ˜5 mmHg) weight loss: goal BMI 18.5-24.9; aerobic exercise: ≥30 min exercise/d, ≥5 d/wk diet: rich in fruits & vegetables, low in saturated & total fat (DASH, NEJM 2001;344:3) sodium restriction: ≤2.4 g/d and ideally ≤1.5 g/d (NEJM 2010;362:2102) maintain adequate potassium intake through diet counseling (˜120 mEq of dietary potassium) if no predisposition to hyperkalemia (NEJM 2007;356:1966)
limit alcohol consumption: ≤2 drinks/d in ♂; ≤1 drink/d in ♀ & lighter-wt Pts avoid exacerbating exposures (eg, NSAID use)
Pharmacologic options for HTN or pre-HTN w/ comorbidity (nb, pre-HTN w/o DM, CKD, CV disease, or other end organ dysfunction treated w/ lifestyle alone) Pre-HTN: ARB prevents onset of HTN, no ↑ in clinical events (NEJM 2006;354:1685) HTN: choice of therapy controversial, concomitant disease and stage may help guide Rx uncomplicated: CCB, ARB or ACEI, or thiazide (chlorthalidone preferred) are 1st line (NEJM 2009;361:2153); βB not 1st line (Lancet 2005;366:1545).
For non-black Pts <60 y: reasonable to start w/ ARB or ACEI, then add CCB or thiazide if needed, and then add remaining class if still needed
For black, elderly, and ? obese Pts (all of whom more likely to be salt sensitive): reasonable to start with CCB or thiazide, then add either the other 1st choice class or ARB or ACEI if needed, and then all 3 classes if still needed
+CAD (Circ 2015;131:e435): ACEI or ARB (NEJM 2008;358:1547); ACEI+CCB superior to ACEI+thiazide (NEJM 2008;359:2417) or βB+diuretic (Lancet 2005;366:895); may require βB and/or nitrates for anginal relief; if h/o MI, βB ± ACEI/ARB ± aldo antag (see “ACS”)
Tailoring therapy
lifestyle Δs typically complementary rather than alternative to drug Rx [although if low risk (stage 1, no end-organ damage or risk factors), could start with lifestyle]
if stage 1, start w/ monoRx; if stage 2, consider starting w/ combo (eg, ACEI + CCB; NEJM 2008;359:2417), as most will require ≥2 drugs
typically start drug at ½ maximal dose; after 2-3 wk either titrate up or add new drug
Differentiate between true & pseudoresistance, w/ latter due to: inaccurate measurement or use of wrong cuff size poor dietary compliance (Na/K intake, can assess w/ 24-hr urine for Na, K and Cr) suboptimal med dosing (eg, <50% of max dose) or poor med compliance volume expansion (inadequate diuretic dosing) white coat HTN (consider ABPM) 2° causes or external drivers (eg, OSA, steroids, NSAIDS, alcohol) (Lancet 2010;376:1903)
Treatment considerations:
Persistent ↑ volume may contribute even if on standard HCTZ (Archives 2008;168:1159).
Effective diuretic dosing required for most to achieve control (HTN 2002;39:982).
Chlorthalidone over HCTZ (if renal function preserved). Loop diuretic favored over thiazide for initial Rx if eGFR <30; however, adding thiazide to loop can ↑ diuresis if insufficient response to loop alone.
Adding aldosterone antagonist (if renal function preserved) (PATHWAY-2, ESC 2015)
Adding β-blocker (particularly vasodilating ones such as labetalol, carvedilol, or nebivolol), centrally acting agent, α-blocker, or direct vasodilator
Other Rx under investigation: renal denervation (see below); carotid baroreceptor stimulation; central AV anastomosis ↑ SBP by ˜23 mmHg (Lancet 2015;385:1634)
Secondary causes
Renovascular (qv)
Renal parenchymal disease: salt and fluid restriction, ± diuretics
Endocrine etiologies: see “Adrenal Disorders”
Hypertensive emergency: ↑ BP → acute target-organ ischemia and damage
neurologic: encephalopathy (insidious onset of headache, nausea, vomiting, confusion), hemorrhagic or ischemic stroke, papilledema
renal: proteinuria, hematuria, acute renal failure; scleroderma renal crisis
microangiopathic hemolytic anemia; preeclampsia-eclampsia
Tailor goals to clinical context (eg, more rapid lowering for Ao dissection)
Emergency: ↓ MAP by ˜25% in mins to 2 h w/ IV agents (may need arterial line for monitoring); goal DBP <110 w/in 2-6 h, as tolerated
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Atherosclerosis (˜90%): usually involving ostial or prox segments. Often incidental finding as common in Pts w/ established athero (eg, CAD, PAD) but uncommon cause of HTN.
Fibromusclar dysplasia (FMD, ˜10%): nonathero medial fibroplasia usually mid/distal female-predominant (85-90%); mean age 52 y (Circ 2012;125:3182) characteristic “string of beads” appearance (or concentric smooth stenosis) on angio usually > 1 territory involved (eg, carotid in ˜65%), explaining sx of HA, dizziness, tinnitus
Consider testing if any of the following and if finding would modify treatment:
Clinical picture consistent w/ secondary HTN w/ no other compelling etiology Severe HTN (SBP ≥180 and/or DBP ≥120 mmHg) and/or flash pulm edema/CHF Progressive renal insufficiency w/ bland sediment, unilateral small kidney (≤9 cm), renal asymmetry > 1.5 cm, or acute sustained Cr ↑ by ≥30% w/in 1 wk of starting ACEI/ARB
Testing for Renovascular Disease (Am Fam Physician 2009;80:273)
Modality
Notes
Duplex Doppler US
85%
92%
Pt habitus & operator dependent. May be preferred if renal dysfxn. Allows quantification of resistive index.*
88-96%
97%
Less sensitive (˜30%) for distal disease such as FMD Contrast agent nephrotoxic
88-100%
>95%
Less sensitive (˜30%) for distal disease such as FMD Risk of nephrogenic systemic fibrosis if mod-sev CKD
Angiography (DSA)
gold standard
Allows measurement of gradients Invasive, contrast agent nephrotoxic
Plasma Renin Activity (PRA)
50-80%
low
Not 1st line. Can ↑ Se by measuring 1 hr after capto administration
Captopril Renal Scan
75-100%
n/a
Not 1st line, but can determine hemodynamic signif of stenosis. Not reliable in bilateral RAS or poor renal fxn.
* Resistive index = [(peak syst vel – end diast vel) / peak syst vel].
Monitoring: for athero, repeat imaging only necessary if Δ in clinical status that would lead to intervention; for FMD image q6-12mo to assess for progression
If due to atherosclerosis, risk factor modification: quit smoking, ↓ chol
Revascularization (typically percutaneous w/ stenting):
However, clinical trials enrolling stable Pts w/ mod stenosis (50-70%) and HTN on ≥2 agents showed no benefit on # of BP meds, renal fxn or CV outcomes (NEJM 2000;342:1007; 2009;361:1953; 2014;370:13). Unknown if beneficial in more severe stenoses or in higher-risk Pts (eg, recent CHF, >3 meds).
Resistive index >80 on U/S implies intrinsic renal damage and thus less likely to benefit from revasc, so may predict outcome after intervention (NEJM 2001;344:410). Operator dependent and some studies have not replicated findings, so not utilized broadly.
Renal vein renin measurements, PRA, captopril renogram may provide supportive evidence as to hemodynamic significance of RAS, but limited utility due to low Se
Surgery (very rare): resection of pressor kidney
Bilateral RAS: 20-46% of Pts w/ RAS. Associated w/ higher creatinine and worse CV outcomes. In addition to anti-HTN Rx, consider revasc if likely to benefit (failure of meds, recurrent pulmonary edema, progressive renal failure). Trials including Pts w/ bilateral RAS did not show benefit but included moderate stenoses.
True aneurysm (≥50% dilation of all 3 layers of aorta; <50% called ectasia) vs false or pseudoaneurysm (rupture contained by adventitia)
Location: root (annuloaortic ectasia), thoracic aortic aneurysm (TAA), thoracoabdominal aortic aneurysm (TAAA), abdominal aortic aneurysm (AAA)
Type: fusiform (circumferential dilation) vs saccular (localized dilation of aortic wall)
Medial degeneration and/or ↑ wall stress
Medial degeneration = muscle apoptosis, elastin fiber weakening, mucoid infiltration
Wall stress ∝ [(ΔP × r) / (wall thickness)], LaPlace’s law
TAA: most commonly medial degeneration; seen w/ connective tissue disorders & aortitis
Marfan syndrome (mutations in fibrillin-1, FBN-1): cardinal features are Ao root aneurysm & ectopia lentis. Other suggestive signs include: tall stature; arachnodactyly w/ thumb sign (entire distal phalanx of adduct. thumb extends beyond ulnar border of palm) and/or wrist sign (tip of thumb covers 5th finger fingernail when wrapped around contralat wrist); pectus deformities; scoliosis; dural ectasia; spontaneous PTX; MVP.
Loeys-Dietz syndrome (mutation in TGF-β receptors 1 or 2, TGFBR1/2): triad of arterial tortuosity & aneurysms, widely spaced eyes, bifid uvula or cleft palate. Also w/ velvety & hyperlucent skin and bluish sclera.
Vascular Ehlers-Danlos syndrome (mutation in type III procollagen, COL3A1): easy bruising; thin, translucent skin w/ visible veins (but not excessively stretchable); acrogeria (aged appearance of hands & feet); flexible digits; uterine or intestinal rupture; distinctive facial features (protruding eyes, thin nose & lips, sunken cheeks, small chin)
Other genetic disorders: bicuspid AoV; Turner syndrome (45X; short stature, ovarian failure, Ao coarctation); other familial aortopathies (mutations in smooth muscle myosin & actin genes including MYH11 and ACTA2)
Aortitis: Takayasu’s, GCA, spondyloarthritis, IgG4-related disease
Infection (ie, mycotic aneurysm): salmonella, TB, syphilis
Goal is to prevent rupture (50% mortality prior to hospital) by modifying risk factors
Statin (to achieve LDL-C <70 mg/dL): ↓ death and stroke & possibly ↓ rate of expansion (Eur J Vasc Endovasc Surg 2006;32:21)
ARB may ↓ rate of aortic root growth in Marfan (NEJM 2008;358:2787)
βB and ARB similar ↓ rate of Ao root growth in children and young adults w/ Marfan (NEJM 2014;371:2061)
Moderate cardiovascular exercise okay, but no burst activity/exercise requiring Valsalva maneuvers (eg, heavy lifting)
Indications for intervention (surgery/endovascular repair)
Individualize based on FHx, body size, gender, anatomy, surgical risk
TAA (Circ 2010;121:1544 & e266) symptoms
ascending Ao ≥5.5 cm (4-5 cm if Marfan, bicuspid AoV, Loeys-Dietz, vascular EDS, or other genetic/familial disorder)
descending >6 cm ↑ >0.5 cm/y
aneurysm >4.5 cm and planned AoV surgery
Ascending aorta
No root involvement: resection & replacement w/ Dacron tube graft
Root involvement: need to address AoV integrity; depending on AoV itself: modified Bentall: Dacron Ao root + prosthetic AoV, reattach coronaries valve-sparing: reimplant native AoV in Dacron Ao graft; reattach coronaries
Arch: high-risk, complex surgery because of the arch branches; variety of combinations of partial/complete resection, stent graft & bypass of arch vessels
Descending thoracic aorta: resection & grafting vs endovascular repair (qv)
Depends on favorable aortic anatomy
TEVAR (thoracic EVAR) for descending TAA ≥5.5 cm may ↑ periop morbidity and possibly mortality (Circ 2010;121:2780; JACC 2010;55:986; J Thorac CV Surg 2010;140:1001 & 2012;144:604)
Guidelines support open repair or EVAR for infrarenal AAA in good surg candidates ↓ short-term mort., bleeding, LOS; but long-term graft complic. (3-4%/y; endoleak, need for reintervention, rupture) necessitate periodic surveillance, with no proven Δ in overall mortality in trials, except ? in those <70 y (NEJM 2010;362:1863, 1881 & 2012;367:1988)
In observational data, EVAR assoc w/ ↑ survival over 1st 3 y, after which survival similar. Rates of rupture over 8 y 5.4% w/ EVAR vs 1.4% w/ surgery (NEJM 2015;373:328)
In Pts unfit for surgery or high periop risks: ↓ aneurysm-related mortality but no Δ in overall mortality over medical Rx (NEJM 2010;362:1872). EVAR noninferior (? superior) to open repair in ruptured AAA w/ favorable anatomy (Ann Surg 2009;250:818).
Pt selection for endovascular includes requirement to comply with long-term surveillance
Pain: gnawing chest, back or abdominal pain; new or worse pain may signal rupture
AAA: ˜1%/y if <5 cm vs 6.5%/y if 5-5.9 cm rupture p/w severe constant pain and hemorrhagic shock; ˜80% mortality at 24 h
Aortic insufficiency (TAA) and CHF
Acute aortic syndromes (qv)
Thromboembolic ischemic events (eg, to CNS, viscera, extremities)
Compression of adjacent structures (eg, SVC, trachea, esophagus, laryngeal nerve)
Aortic dissection (AoD): intimal tear → blood extravasates into Ao media (creates false lumen). Rate 3-16/100,000 Pt-yrs. False lumen acts as “wind sock,” ↑ in size and compressing true lumen (patency of false lumen associated with outcome).
Intramural hematoma (IMH): vasa vasorum rupture → medial hemorrhage that does not communicate with aortic lumen; 6% of aortic syndromes; clinically managed as AoD
Proximal: involves ascending Ao, regardless of origin (= Stanford A, DeBakey I & II)
Distal: involves descending Ao only, distal to L subclavian art. (= Stanford B, DeBakey III)
Other Considerations: isolated to arch generally treated as proximal; distal with involvement of subclavian depends on overall clinical picture.
Classic (in older Pts): hypertension (h/o HTN in >70% of dissections); age (60s-70s), male sex (˜70% ♂); smoking
Genetic or acquired predisposition (may present younger; see “Aortic Aneurysms”):
Connective tissue disease/congenital anomaly: Marfan, Loeys-Dietz, vascular Ehlers-Danlos, bicuspid AoV, coarctation (eg, in Turner’s), other familial aortopathies, PCKD
Aortitis: Takayasu’s, GCA, Behçet’s, syphilis
Pregnancy: typically 3rd trimester
Other environmental factors:
Trauma: blunt, deceleration injury
Cardiovascular procedures: IABP, cardiac or aortic surgery, cardiac catheterization
Acute ↑ BP: cocaine, Valsalva (eg, weightlifting)
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