Vascular Disease



Vascular Disease





HYPERTENSION
































Classification


Category

Systolic (mmHg)

Diastolic (mmHg)


Normal

<120

<80


Pre-HTN

120-139

80-89


Stage 1 HTN

140-159

90-99


Stage 2 HTN

≥160

≥100


Average ≥2 measurements >1-2 min apart. Confirm stage 1 w/in 1-4 wk; can Rx stage 2 immediately. [check mark] q2y (if nl) or yearly (if pre-HTN). (J Clin HTN 2014;16:14)





























Ambulatory Thresholds


Setting

Systolic (mmHg)

Diastolic (mmHg)


24-hr average

135

85


Day* (awake)

140

90


Night (asleep)

125

75


* Threshold of hypertension for home readings should be same as daytime ambulatory



Epidemiology (Circulation 2012;125:e2)



  • 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


  • Only 48% of patients with dx of HTN have adequate BP control


Etiologies



  • 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


  • Secondary: Consider if Pt <20 or >50 y or if sudden onset, severe, refractory HTN
















































Secondary Causes of Hypertension


Diseases

Suggestive findings

Initial workup


RENAL

Renal parenchymal (2-3%)

h/o DM, polycystic kidney disease, glomerulonephritis

CrCl, albuminuria See “Renal Failure”


Renovascular (1-2%, qv) Athero (90%) FMD (10%, women) PAN, scleroderma

ARF induced by ACEI/ARB Recurrent flash pulm edema Renal bruit; hypokalemia (NEJM 2009;361:1972)

MRA (>90% Se & Sp, less for FMD), CTA, duplex U/S, angio, plasma renin (low Sp)


ENDO

Hyperaldo or Cushing’s (1-5%)

Hypokalemia Metabolic alkalosis

See “Adrenal Disorders”


Pheochromocytoma (<1%)

Paroxysmal HTN, H/A, palp.


Myxedema (<1%)

See “Thyroid Disorders”

TFTs


Hypercalcemia (<1%)

Polyuria, dehydration, Δ MS

iCa


OTHER

Obstructive sleep apnea (qv)


Medications: OCP, steroids, licorice; NSAIDs (espec COX-2); Epo; cyclosporine


Aortic coarctation: ↓ LE pulses, systolic murmur, radial-femoral delay; abnl TTE, CXR


Polycythemia vera: ↑ Hct



Standard workup (J Clin HTN 2014;16:14)



  • Goals: (1) identify CV risk factors or other diseases that would modify prognosis or Rx;

    (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).


Complications of HTN



  • Each ↑ 20 mmHg SBP or 10 mmHg DBP → 2× → CV complications (Lancet 2002;360:1903)


  • Neurologic: TIA/CVA, ruptured aneurysms, vascular dementia



  • Retinopathy: stage I = arteriolar narrowing; II = copper wiring, AV nicking; III = hemorrhages and exudates; IV = papilledema


  • Cardiac: CAD, LVH, HF, AF


  • Vascular: aortic dissection, aortic aneurysm (HTN = key risk factor for aneurysms)


  • Renal: proteinuria, renal failure



Treatment (JAMA 2014;311:507; J Clin HTN 2014;16:14; JACC 2015;65:1998)



  • 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/ prior MI or stroke: reasonable to consider <130/80 (HTN 2015;65:1372)

    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)


  • Treatment results in 50% ↓ HF, 40% ↓ stroke, 20-25% ↓ MI (Lancet 2014;384:591)


  • 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”)

    +HF: ACEI/ARB, βB, diuretics, aldosterone antagonist (see “Heart Failure”)

    +2° stroke prevention: ACEI (Lancet 2001;358:1033); ? ARB (NEJM 2008;359:1225)

    +diabetes mellitus: ACEI or ARB; can also consider thiazide or CCB

    +chronic kidney disease: ACEI or ARB (NEJM 1993;329:1456 & 2001;345:851 & 861)


  • 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


Resistant hypertension (JAMA 2014;311:2216)



  • BP > goal on ≥3 drugs incl diuretic, ˜12-13% of hypertensive population (HTN 2011;57:1105)


  • 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)


  • True resistance = uncontrolled BP confirmed by ABPM despite compliance w/ optim. doses


  • 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)


  • Renal denervation: catheter-based RF ablation of renal nerves modifying sympathetic outflow. Had appeared beneficial in unblinded and/or uncontrolled studies, but no effect on BP in controlled trial, so not currently an option in routine care (NEJM 2014;370:1393).


Special situations



  • Secondary causes

    Renovascular (qv)

    Renal parenchymal disease: salt and fluid restriction, ± diuretics

    Endocrine etiologies: see “Adrenal Disorders”


  • Pregnancy: methyldopa, labetalol, nifedipine, hydralazine; avoid diuretics; Ø ACEI/ARB


HYPERTENSIVE CRISES



  • Hypertensive emergency: ↑ BP → acute target-organ ischemia and damage

    neurologic: encephalopathy (insidious onset of headache, nausea, vomiting, confusion), hemorrhagic or ischemic stroke, papilledema

    cardiac: ACS, HF/pulmonary edema, aortic dissection

    renal: proteinuria, hematuria, acute renal failure; scleroderma renal crisis

    microangiopathic hemolytic anemia; preeclampsia-eclampsia


  • Hypertensive urgency (severe asymptomatic HTN): SBP >180 or DBP >120 (?110) w/ minimal or no target-organ damage


Precipitants



  • Progression of essential HTN ± medical noncompliance (espec clonidine) or Δ in diet


  • Progression of renovascular disease; acute glomerulonephritis; scleroderma; preeclampsia


  • Endocrine: pheochromocytoma, Cushing’s


  • Sympathomimetics: cocaine, amphetamines, MAO inhibitors + foods rich in tyramine


  • Cerebral injury: do not treat HTN in acute ischemic stroke unless Pt getting lysed, extreme BP (>220/120), Ao dissection, active ischemia or HF (Stroke 2003;34:1056)



Treatment (Chest 2007;131:1949)



  • 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


  • Urgency: ↓ BP to ≤160/100 in hrs using PO agents; goal normal BP in ˜1-2 d


  • Watch UOP, Cr, mental status: may indicate a lower BP is not tolerated



































Drugs for Hypertensive Crises


IV

Nitroprusside* 0.25-10 mcg/kg/min

Nitroglycerin 5-1000 mcg/min


Labetalol 20-80 mg IVB q10min or 0.5-2 mg/min

Esmolol 0.5 mg/kg load → 0.05-0.2 mg/kg/min


Fenoldopam 0.1-1.6 mcg/kg/min

Hydralazine 10-20 mg q20-30 min


Nicardipine 5-15 mg/h

Clevidipine 1-16 mg/h


Phentolamine 5-15 mg bolus q5-15min

Enalaprilat 1.25 mg


PO

Captopril 12.5-100 mg tid

Labetalol 200-800 mg tid


Clonidine 0.2 mg load → 0.1 mg qh

Hydralazine 10-75 mg qid


* Metabolized to cyanide → Δ MS, lactic acidosis, death. Limit use of very high doses (8-10 mcg/kg/min) to <10 min. Monitor thiocyanate levels. Hydroxocobalamin or sodium thiosulfate infusion for treatment of cyanide toxicity.



































Treatment Considerations for Specific Clinical Settings


Clinical

Setting Note

Treatment


Acute stroke

BP ↓ must be balanced w/ risk of worsening ischemia

Consult stroke team


Aortic dissection (qv)

[check mark] BP in both arms and treat higher value

βB first, then add vasodilator (eg, nitroprusside) if needed


Acute pulm edema

Avoid [circled dash] inotropes (eg, βB) if LV dysfxn, unless ischemia

Vasodilator (eg, NTG) and loop diuretic


Antihypertensive withdrawal

Suspect if abrupt d/c of symp. blocker (eg, clonidine)

Restart d/c’d drug or consider labetalol or nitroprusside


Sympathetic activity (pheo, auton dysfxn, cocaine, MAO + tyramine-containing foods)

Avoid βB as could → unopposed α in vasculature → vasconstriction and further ↑ BP

Phentolamine (pheochromocytoma), nitroprusside




RENOVASCULAR DISEASE



Pathophysiology



  • ↑ renal perfusion → activation of RAA system → vasoconstriction, ↑ aldo & vasopressin, ↑ sympathetic activity → volume retention & HTN → progressive renal dysfxn and CV risk


  • Unilateral stenosis ↑ HTN


  • Bilateral (or unilat involving solitary functioning kidney) → HTN & progressive renal insuffic


Etiologies



  • 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


  • Other (uncommon): vasculitis (Takayasu’s, GCA, PAN or eosinophilic granulomatosis w/ polyangiitis) often w/ ↑ inflammatory markers, systemic s/s; scleroderma; local aneurysm or dissection; embolism; retroperitoneal fibrosis



Diagnosis



  • 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

    Se

    Sp

    Notes


    Duplex Doppler US

    85%

    92%

    Pt habitus & operator dependent. May be preferred if renal dysfxn. Allows quantification of resistive index.*


    CTA

    88-96%

    97%

    Less sensitive (˜30%) for distal disease such as FMD Contrast agent nephrotoxic


    MRA

    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



Treatment



  • If due to atherosclerosis, risk factor modification: quit smoking, ↓ chol


  • Antihypertensive Rx effective for most Pts: diuretic + ACEI/ARB (watch for ↑ Cr) or CCB


  • Revascularization (typically percutaneous w/ stenting):

    Had considered if refractory HTN, recurrent flash pulm edema, worsening CKD

    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

    For FMD (usually more distal lesions): PTA ± bailout stenting


  • 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.



AORTIC ANEURYSMS



Definitions



  • 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)


Epidemiology (Circ 2010;121:e266, 2011;124:2020 & 2013;127:e6; Nat Rev Cardiol 2011;8:92)



  • In U.S., ˜15,000 deaths/y from aortic ruptures; overall ˜50,000 deaths/y from Ao disease


  • TAA: 10/100,000 Pt-yrs, ♂:♀ 2:1; ˜60% root/ascending; 40% descending


  • AAA: ˜4-8% prev in those >60 y (although may be ↓ ; Circ 2011;124:1118); 4-6× more common in ♂ vs ♀; mostly infrarenal


  • Arch & TAAA rarer



Pathophysiology (NEJM 2009;361:1114; Nat Med 2009;15:649)



  • 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


  • AAA: most commonly long-standing HTN + athero/inflammation → medial weakening


Risk factors



  • Classic: HTN, atherosclerosis, smoking, age, male sex


  • 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


Screening (Circ 2010;121:e266 & 2011;124:2020; Annals 2014;161:281; JAMA 2015;313:1156)



  • TAA: if bicuspid AoV or 1° relative w/: (a) TAA or bicuspid valve, (b) Marfan, Loeys-Dietz, Turner; known relevant genetic mutation (see above)


  • AAA: [check mark] for pulsatile abd mass; U/S ♂ >60 y w/ FHx of AAA & ♂ 65-75 y w/ prior tobacco


Diagnostic studies (Circ 2010;121:e266 & 2011;124:2020)



  • Contrast CT: quick, noninvasive, high Se & Sp for all aortic aneurysms


  • TTE/TEE: TTE most useful for root and proximal Ao; TEE can visualize other sites of TAA


  • MRI: preferred over CT for aortic root imaging for TAA; also useful in AAA but time-consuming; noncontrast “black blood” MR to assess aortic wall


  • Abdominal U/S: screening and surveillance test of choice for infrarenal AAA


Treatment principles (Circ 2006;113:e463; 2008;117:1883; 2010;121:1544 & e266)



  • Goal is to prevent rupture (50% mortality prior to hospital) by modifying risk factors


  • Smoking cessation: smoking associated w/ ↑ rate of expansion (Circ 2004;110:16)


  • Statin (to achieve LDL-C <70 mg/dL): ↓ death and stroke & possibly ↓ rate of expansion (Eur J Vasc Endovasc Surg 2006;32:21)


  • BP control: βB (↓ dP/dt) ↓ aneurysm growth (NEJM 1994;330:1335)

    ACEI a/w ↓ risk of rupture (Lancet 2006;368:659)

    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

    AAA (NEJM 2002;346:1437 & 2014;371:2101) symptoms infrarenal ≥5.5 cm, but consider ≥5.0 cm in ♀ ↑ >0.5 cm/y; inflam/infxn


Surgery (Circ 2010;121:e266; EHJ 2014;25:2873)



  • 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)


Endovascular repair (EVAR) (NEJM 2008;358:494; Circ 2011;124:2020 & 2015;131:1291)



  • 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)


  • AAA

    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



Complications (Circ 2010;121:e266; Nat Rev Cardiol 2011;8:92)



  • Pain: gnawing chest, back or abdominal pain; new or worse pain may signal rupture


  • Rupture: risk ↑ w/ diameter, ♀, current smoking, HTN

    TAA: ˜2.5%/y if <6 cm vs 7%/y if >6 cm

    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)


Follow-up (Circ 2010;121:1544 & e266; Nat Rev Cardiol 2011;8:92; JAMA 2013;309:806)



  • Expansion rate ˜0.1 cm/y for TAA, ˜0.3-0.4 cm/y for AAA


  • AAA: <4 cm q2-3 yrs; 4-5.4 cm q6-12 mos; more frequent if rate of expansion >0.5 cm in 6 mo


  • TAA: 6 mo after dx to ensure stable, and if stable, then annually (Circ 2005;111:816)


  • Screen for CAD, PAD and aneurysms elsewhere, espec popliteal. About 25% of Pts w/ TAA will also have AAA, and 25% of AAA Pts will have a TAA: consider pan-Ao imaging.


  • Patients with endovascular repair require long-term surveillance for endoleak & to document stability of aneurysm



ACUTE AORTIC SYNDROMES



Definitions (Circ 2005,112:3802 & 2010;121:e266; Eur Heart J 2012;33:26)



  • 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


  • Penetrating ulcer (PAU): atherosclerotic plaque penetrates elastic lamina → medial hemorrhage. PAU in setting of IMH assoc. w/ similar outcomes as AoD. Outcomes for isolated PAU less well defined but considered AAS. Rx depends on clinical context.


Classification (proximal twice as common as distal)



  • 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.


Risk factors



  • 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)
















































Clinical Manifestations and Physical Exam* (JAMA 2000;283:897)


Feature

Proximal

Distal


“Aortic” pain (abrupt, severe, tearing or ripping quality, maximal at onset [vs crescendo for ACS])

94% (chest, back)

98% (back, chest, abd)


Syncope (often due to tamponade)

13%

4%


HF (usually due to acute AI)

9%

3%


CVA

6%

2%


HTN

36%

70%


HoTN or shock (tamponade, AI, MI, rupture)

25%

4%


Pulse deficit (if involves carotid, subclavian, fem)

19%

9%


AI murmur

44%

12%


* S/S correlate w/ affected branch vessels & distal organs; may Δ as dissection progresses.

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Related posts:

  1. Coronary Disease
  2. Arrhythmias
  3. Coronary Disease
  4. Vascular Disease

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Jun 19, 2016 | Posted by in CARDIOLOGY | Comments Off on Vascular Disease

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